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Gene Information
Gene symbol: BCL2
Gene name: B-cell CLL/lymphoma 2
HGNC ID: 990
Synonyms: Bcl-2, PPP1R50
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 7589882 | Low bcl-2 expression and increased spontaneous apoptosis in T-lymphocytes from newly-diagnosed IDDM patients. |
| 2 | 7589882 | No data exist regarding bcl-2 expression in autoimmune diseases, such as human insulin-dependent diabetes mellitus (IDDM). |
| 3 | 7589882 | We investigated bcl-2 protein expression by testing T lymphocytes from 15 newly-diagnosed (< 3 weeks) IDDM patients in comparison to 10 age-matched control subjects. |
| 4 | 7589882 | When the percentage and mean fluorescence intensity (MFI) of bcl-2+/CD3+ cells from normal individuals and patients were compared, we found that bcl-2 expression within the CD3+ and CD4+ CD45R0+ T-cell populations was reduced significantly in IDDM patients (46.8 +/- 15.4 vs 79.6 +/- 11.7; 25.7 +/- 3.8 vs 47.15 +/- 5.7, respectively; p < 0.001). |
| 5 | 7589882 | Our study suggests that recent onset IDDM is characterised by reduced bcl-2 expression, which in turn may be associated with the increased spontaneous apoptosis we observed. |
| 6 | 7589882 | Low bcl-2 expression and increased spontaneous apoptosis in T-lymphocytes from newly-diagnosed IDDM patients. |
| 7 | 7589882 | No data exist regarding bcl-2 expression in autoimmune diseases, such as human insulin-dependent diabetes mellitus (IDDM). |
| 8 | 7589882 | We investigated bcl-2 protein expression by testing T lymphocytes from 15 newly-diagnosed (< 3 weeks) IDDM patients in comparison to 10 age-matched control subjects. |
| 9 | 7589882 | When the percentage and mean fluorescence intensity (MFI) of bcl-2+/CD3+ cells from normal individuals and patients were compared, we found that bcl-2 expression within the CD3+ and CD4+ CD45R0+ T-cell populations was reduced significantly in IDDM patients (46.8 +/- 15.4 vs 79.6 +/- 11.7; 25.7 +/- 3.8 vs 47.15 +/- 5.7, respectively; p < 0.001). |
| 10 | 7589882 | Our study suggests that recent onset IDDM is characterised by reduced bcl-2 expression, which in turn may be associated with the increased spontaneous apoptosis we observed. |
| 11 | 7589882 | Low bcl-2 expression and increased spontaneous apoptosis in T-lymphocytes from newly-diagnosed IDDM patients. |
| 12 | 7589882 | No data exist regarding bcl-2 expression in autoimmune diseases, such as human insulin-dependent diabetes mellitus (IDDM). |
| 13 | 7589882 | We investigated bcl-2 protein expression by testing T lymphocytes from 15 newly-diagnosed (< 3 weeks) IDDM patients in comparison to 10 age-matched control subjects. |
| 14 | 7589882 | When the percentage and mean fluorescence intensity (MFI) of bcl-2+/CD3+ cells from normal individuals and patients were compared, we found that bcl-2 expression within the CD3+ and CD4+ CD45R0+ T-cell populations was reduced significantly in IDDM patients (46.8 +/- 15.4 vs 79.6 +/- 11.7; 25.7 +/- 3.8 vs 47.15 +/- 5.7, respectively; p < 0.001). |
| 15 | 7589882 | Our study suggests that recent onset IDDM is characterised by reduced bcl-2 expression, which in turn may be associated with the increased spontaneous apoptosis we observed. |
| 16 | 7589882 | Low bcl-2 expression and increased spontaneous apoptosis in T-lymphocytes from newly-diagnosed IDDM patients. |
| 17 | 7589882 | No data exist regarding bcl-2 expression in autoimmune diseases, such as human insulin-dependent diabetes mellitus (IDDM). |
| 18 | 7589882 | We investigated bcl-2 protein expression by testing T lymphocytes from 15 newly-diagnosed (< 3 weeks) IDDM patients in comparison to 10 age-matched control subjects. |
| 19 | 7589882 | When the percentage and mean fluorescence intensity (MFI) of bcl-2+/CD3+ cells from normal individuals and patients were compared, we found that bcl-2 expression within the CD3+ and CD4+ CD45R0+ T-cell populations was reduced significantly in IDDM patients (46.8 +/- 15.4 vs 79.6 +/- 11.7; 25.7 +/- 3.8 vs 47.15 +/- 5.7, respectively; p < 0.001). |
| 20 | 7589882 | Our study suggests that recent onset IDDM is characterised by reduced bcl-2 expression, which in turn may be associated with the increased spontaneous apoptosis we observed. |
| 21 | 7589882 | Low bcl-2 expression and increased spontaneous apoptosis in T-lymphocytes from newly-diagnosed IDDM patients. |
| 22 | 7589882 | No data exist regarding bcl-2 expression in autoimmune diseases, such as human insulin-dependent diabetes mellitus (IDDM). |
| 23 | 7589882 | We investigated bcl-2 protein expression by testing T lymphocytes from 15 newly-diagnosed (< 3 weeks) IDDM patients in comparison to 10 age-matched control subjects. |
| 24 | 7589882 | When the percentage and mean fluorescence intensity (MFI) of bcl-2+/CD3+ cells from normal individuals and patients were compared, we found that bcl-2 expression within the CD3+ and CD4+ CD45R0+ T-cell populations was reduced significantly in IDDM patients (46.8 +/- 15.4 vs 79.6 +/- 11.7; 25.7 +/- 3.8 vs 47.15 +/- 5.7, respectively; p < 0.001). |
| 25 | 7589882 | Our study suggests that recent onset IDDM is characterised by reduced bcl-2 expression, which in turn may be associated with the increased spontaneous apoptosis we observed. |
| 26 | 8053485 | Two lytic gene products are of special interest because of their homology to the cellular proteins BCL-2 and interleukin-10. |
| 27 | 8299687 | Consistent with the anti-apoptotic function of the Bcl-2 gene product, activated T lymphocytes from NOD mice showed a markedly increased resistance to induction of apoptosis following deprivation of interleukin-2 when compared to those from non-autoimmune strains. |
| 28 | 9292301 | Bcl-2 and p53 protein expression in aortic, mammary artery and saphenous vein biopsies in patients subjected to open heart surgery. |
| 29 | 9492080 | Altered bcl-2 and bax expression and intracellular Ca2+ signaling in apoptosis of pancreatic cells and the impairment of glucose-induced insulin secretion. |
| 30 | 9519752 | In this study, we sought evidence for diabetes-induced Müller cell abnormalities by testing the expression of three proteins (Bcl-2, glutamine synthetase [GS], and glial fibrillar acidic protein [GFAP]) that are solely or predominantly expressed in Müller cells and show a reproducible pattern of changes in the context of retinal injuries or degenerations. |
| 31 | 9654911 | Bax product, an inducer of apoptosis, and Bcl-2 protein, an inhibitor of apoptosis, were examined immunohistochemically in the seven autopsied renal tissues with amyloidosis and 10 autopsied control tissues. |
| 32 | 9689119 | Protection against lipoapoptosis of beta cells through leptin-dependent maintenance of Bcl-2 expression. |
| 33 | 9689119 | Leptin completely blocked FA-induced Bcl-2 suppression in normal islets but had no effect on islets from fa/fa rats, which are unresponsive to leptin because of a mutation in their leptin receptors (OB-R). |
| 34 | 9689119 | However, when wild-type OB-R is overexpressed in fa/fa islets, leptin completely prevented FA-induced Bcl-2 suppression and DNA fragmentation. |
| 35 | 9689119 | Protection against lipoapoptosis of beta cells through leptin-dependent maintenance of Bcl-2 expression. |
| 36 | 9689119 | Leptin completely blocked FA-induced Bcl-2 suppression in normal islets but had no effect on islets from fa/fa rats, which are unresponsive to leptin because of a mutation in their leptin receptors (OB-R). |
| 37 | 9689119 | However, when wild-type OB-R is overexpressed in fa/fa islets, leptin completely prevented FA-induced Bcl-2 suppression and DNA fragmentation. |
| 38 | 9689119 | Protection against lipoapoptosis of beta cells through leptin-dependent maintenance of Bcl-2 expression. |
| 39 | 9689119 | Leptin completely blocked FA-induced Bcl-2 suppression in normal islets but had no effect on islets from fa/fa rats, which are unresponsive to leptin because of a mutation in their leptin receptors (OB-R). |
| 40 | 9689119 | However, when wild-type OB-R is overexpressed in fa/fa islets, leptin completely prevented FA-induced Bcl-2 suppression and DNA fragmentation. |
| 41 | 9690053 | A second target is the T cell, and strategies rely on a gene transfer approach to switch on T-cell apoptosis using Fas ligand, or to modulate T-cell populations with cytokines. |
| 42 | 9690053 | Data using transfer of various genes (bcl-2, adenovirus E3, catalase, HSP70) have shown promising perspectives. |
| 43 | 9783328 | Moreover, immunoblot analysis showed high Bcl-2 and undetectable caspase-1 levels in embryos from both normal and diabetic rats and low Bcl-2 and high caspase-1 levels in the corresponding yolk sacs. |
| 44 | 9856487 | An in vitro expression study with a mouse IL-7-dependent pre-B cell line has revealed that inhibition of the programmed cell death function of 43Thr bcl-2 protein is suppressed compared with that of normal 43Ala bcl-2 protein. |
| 45 | 9856487 | To evaluate the clinical impact of this polymorphism, the frequency of bcl-2 polymorphism was investigated in 221 children with insulin-dependent diabetes mellitus (IDDM), 237 adults with autoimmune disease (105 with rheumatoid arthritis, 57 with systemic lupus erythematosus, 55 with Sjögren's syndrome, and 20 others), and 290 healthy Japanese children and adults. |
| 46 | 9856487 | The frequency of the 43Thr bcl-2 allele, either homozygous or heterozygous, was 14.5% in normal controls, 6.8% (P<0.01) in children with IDDM, and 8.0% (P<0.025) in adults with autoimmune disease. |
| 47 | 9856487 | An in vitro expression study with a mouse IL-7-dependent pre-B cell line has revealed that inhibition of the programmed cell death function of 43Thr bcl-2 protein is suppressed compared with that of normal 43Ala bcl-2 protein. |
| 48 | 9856487 | To evaluate the clinical impact of this polymorphism, the frequency of bcl-2 polymorphism was investigated in 221 children with insulin-dependent diabetes mellitus (IDDM), 237 adults with autoimmune disease (105 with rheumatoid arthritis, 57 with systemic lupus erythematosus, 55 with Sjögren's syndrome, and 20 others), and 290 healthy Japanese children and adults. |
| 49 | 9856487 | The frequency of the 43Thr bcl-2 allele, either homozygous or heterozygous, was 14.5% in normal controls, 6.8% (P<0.01) in children with IDDM, and 8.0% (P<0.025) in adults with autoimmune disease. |
| 50 | 9856487 | An in vitro expression study with a mouse IL-7-dependent pre-B cell line has revealed that inhibition of the programmed cell death function of 43Thr bcl-2 protein is suppressed compared with that of normal 43Ala bcl-2 protein. |
| 51 | 9856487 | To evaluate the clinical impact of this polymorphism, the frequency of bcl-2 polymorphism was investigated in 221 children with insulin-dependent diabetes mellitus (IDDM), 237 adults with autoimmune disease (105 with rheumatoid arthritis, 57 with systemic lupus erythematosus, 55 with Sjögren's syndrome, and 20 others), and 290 healthy Japanese children and adults. |
| 52 | 9856487 | The frequency of the 43Thr bcl-2 allele, either homozygous or heterozygous, was 14.5% in normal controls, 6.8% (P<0.01) in children with IDDM, and 8.0% (P<0.025) in adults with autoimmune disease. |
| 53 | 10342808 | The bcl-2-transfected beta-cells were fully protected from impaired insulin secretion and destruction resulting from incubation for 5 days with the cytokine combination of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma. |
| 54 | 10426400 | Members of the Bcl-2 family of apoptosis regulatory molecules; Bcl-2 and Bcl-x, appear to have some role in regulating apoptosis in the terminal endbud. |
| 55 | 10455420 | Lentivirus-mediated Bcl-2 expression in betaTC-tet cells improves resistance to hypoxia and cytokine-induced apoptosis while preserving in vitro and in vivo control of insulin secretion. |
| 56 | 10455420 | In this study we genetically engineered betaTC-tet cells with the anti-apoptotic gene Bcl-2 using new lentiviral vectors and showed that it protected this cell line against apoptosis induced by hypoxia, staurosporine and a mixture of cytokines (IL-1beta, IFN-gamma and TNF-alpha). |
| 57 | 10455420 | Expression of Bcl-2, however, did not inter- fere either with the intrinsic mechanism of growth arrest present in the betaTC-tet cells or with their normal glucose dose-dependent insulin secretory activity. |
| 58 | 10455420 | Furthermore, Bcl-2 expressing betaTC-tet cells retained their capacity to secrete insulin under mild hypoxia. |
| 59 | 10455420 | Lentivirus-mediated Bcl-2 expression in betaTC-tet cells improves resistance to hypoxia and cytokine-induced apoptosis while preserving in vitro and in vivo control of insulin secretion. |
| 60 | 10455420 | In this study we genetically engineered betaTC-tet cells with the anti-apoptotic gene Bcl-2 using new lentiviral vectors and showed that it protected this cell line against apoptosis induced by hypoxia, staurosporine and a mixture of cytokines (IL-1beta, IFN-gamma and TNF-alpha). |
| 61 | 10455420 | Expression of Bcl-2, however, did not inter- fere either with the intrinsic mechanism of growth arrest present in the betaTC-tet cells or with their normal glucose dose-dependent insulin secretory activity. |
| 62 | 10455420 | Furthermore, Bcl-2 expressing betaTC-tet cells retained their capacity to secrete insulin under mild hypoxia. |
| 63 | 10455420 | Lentivirus-mediated Bcl-2 expression in betaTC-tet cells improves resistance to hypoxia and cytokine-induced apoptosis while preserving in vitro and in vivo control of insulin secretion. |
| 64 | 10455420 | In this study we genetically engineered betaTC-tet cells with the anti-apoptotic gene Bcl-2 using new lentiviral vectors and showed that it protected this cell line against apoptosis induced by hypoxia, staurosporine and a mixture of cytokines (IL-1beta, IFN-gamma and TNF-alpha). |
| 65 | 10455420 | Expression of Bcl-2, however, did not inter- fere either with the intrinsic mechanism of growth arrest present in the betaTC-tet cells or with their normal glucose dose-dependent insulin secretory activity. |
| 66 | 10455420 | Furthermore, Bcl-2 expressing betaTC-tet cells retained their capacity to secrete insulin under mild hypoxia. |
| 67 | 10455420 | Lentivirus-mediated Bcl-2 expression in betaTC-tet cells improves resistance to hypoxia and cytokine-induced apoptosis while preserving in vitro and in vivo control of insulin secretion. |
| 68 | 10455420 | In this study we genetically engineered betaTC-tet cells with the anti-apoptotic gene Bcl-2 using new lentiviral vectors and showed that it protected this cell line against apoptosis induced by hypoxia, staurosporine and a mixture of cytokines (IL-1beta, IFN-gamma and TNF-alpha). |
| 69 | 10455420 | Expression of Bcl-2, however, did not inter- fere either with the intrinsic mechanism of growth arrest present in the betaTC-tet cells or with their normal glucose dose-dependent insulin secretory activity. |
| 70 | 10455420 | Furthermore, Bcl-2 expressing betaTC-tet cells retained their capacity to secrete insulin under mild hypoxia. |
| 71 | 10684857 | CD40 ligand (CD154) triggers a short-term CD4(+) T cell activation response that results in secretion of immunomodulatory cytokines and apoptosis. |
| 72 | 10684857 | Signals generated through CD28-B7 and CD40 ligand (CD40L)-CD40 interactions have been shown to be crucial for the induction of long-term allograft survivability. |
| 73 | 10684857 | To investigate potential mechanisms of CD40L-induced allograft acceptance, we coimmobilized hu5C8 with suboptimal amounts of anti-CD3 to stimulate CD4(+) T cells. |
| 74 | 10684857 | We now report that anti-CD3/CD40L costimulation results in CD28-independent activation and subsequent deletion of resting T cells. |
| 75 | 10684857 | Coligation of CD3 and CD40L increased expression of CD69, CD25, and CD54 on CD4(+) T cells. |
| 76 | 10684857 | We also found that costimulation with anti-CD3/CD40L resulted in enhanced production of interleukin (IL)-10, interferon gamma, and tumor necrosis factor alpha but not IL-2 or IL-6. |
| 77 | 10684857 | Consistent with that observation, anti-CD3/CD40L did not enhance the antiapoptotic proteins Bcl-2 and Bcl-xL. |
| 78 | 10684857 | Further, the addition of CD28 at 24 h failed to rescue those cells induced to die after costimulation with anti-CD3/CD40L. |
| 79 | 10760214 | Expression and localization of p53 and bcl-2 in healing wounds in diabetic and nondiabetic mice. |
| 80 | 10760214 | Another protein, bcl-2, is antagonistic to p53 and prevents apoptosis. |
| 81 | 10760214 | The purpose of this study was to determine the expression and location of p53 and bcl-2 mRNA and protein in healing wounds of normal and genetically diabetic mice. |
| 82 | 10760214 | At various time points, full-thickness skin wounds from nondiabetic and diabetic mice were evaluated for p53 and bcl-2 by immunohistochemistry and in situ hybridization. |
| 83 | 10760214 | Messenger RNA for p53 and bcl-2 were quantitated by competitive reverse transcriptase-polymerase chain reaction. |
| 84 | 10760214 | Protein and mRNA for p53 were expressed in the leading edge of migrating epithelium, with apoptosis patterns closely following those of p53 production. p53 mRNA levels decreased soon after wounding, but after a few days, levels increased to greater than baseline. bcl-2 was localized to the wound epithelium, but relative amounts tended to oppose levels of p53, i.e, when p53 increased, bcl-2 decreased and vice versa. |
| 85 | 10760214 | Wounds in diabetic animals showed a delayed onset of p53 mRNA expression but had persistently greater levels for longer periods of time. bcl-2 mRNA expression was further delayed in diabetic mice and did not develop to levels as high as p53. |
| 86 | 10760214 | Our data show that immediately after wounding, bcl-2 increases and p53 decreases to allow for the cellular proliferation that is required for tissue repair. |
| 87 | 10760214 | Over time, bcl-2 levels decrease while p53 levels increase to shut down the inflammatory process and down-regulate the proliferative response. |
| 88 | 10760214 | Diabetic animals appear to lose the indirect relationship between p53 and bcl-2. |
| 89 | 10760214 | Expression and localization of p53 and bcl-2 in healing wounds in diabetic and nondiabetic mice. |
| 90 | 10760214 | Another protein, bcl-2, is antagonistic to p53 and prevents apoptosis. |
| 91 | 10760214 | The purpose of this study was to determine the expression and location of p53 and bcl-2 mRNA and protein in healing wounds of normal and genetically diabetic mice. |
| 92 | 10760214 | At various time points, full-thickness skin wounds from nondiabetic and diabetic mice were evaluated for p53 and bcl-2 by immunohistochemistry and in situ hybridization. |
| 93 | 10760214 | Messenger RNA for p53 and bcl-2 were quantitated by competitive reverse transcriptase-polymerase chain reaction. |
| 94 | 10760214 | Protein and mRNA for p53 were expressed in the leading edge of migrating epithelium, with apoptosis patterns closely following those of p53 production. p53 mRNA levels decreased soon after wounding, but after a few days, levels increased to greater than baseline. bcl-2 was localized to the wound epithelium, but relative amounts tended to oppose levels of p53, i.e, when p53 increased, bcl-2 decreased and vice versa. |
| 95 | 10760214 | Wounds in diabetic animals showed a delayed onset of p53 mRNA expression but had persistently greater levels for longer periods of time. bcl-2 mRNA expression was further delayed in diabetic mice and did not develop to levels as high as p53. |
| 96 | 10760214 | Our data show that immediately after wounding, bcl-2 increases and p53 decreases to allow for the cellular proliferation that is required for tissue repair. |
| 97 | 10760214 | Over time, bcl-2 levels decrease while p53 levels increase to shut down the inflammatory process and down-regulate the proliferative response. |
| 98 | 10760214 | Diabetic animals appear to lose the indirect relationship between p53 and bcl-2. |
| 99 | 10760214 | Expression and localization of p53 and bcl-2 in healing wounds in diabetic and nondiabetic mice. |
| 100 | 10760214 | Another protein, bcl-2, is antagonistic to p53 and prevents apoptosis. |
| 101 | 10760214 | The purpose of this study was to determine the expression and location of p53 and bcl-2 mRNA and protein in healing wounds of normal and genetically diabetic mice. |
| 102 | 10760214 | At various time points, full-thickness skin wounds from nondiabetic and diabetic mice were evaluated for p53 and bcl-2 by immunohistochemistry and in situ hybridization. |
| 103 | 10760214 | Messenger RNA for p53 and bcl-2 were quantitated by competitive reverse transcriptase-polymerase chain reaction. |
| 104 | 10760214 | Protein and mRNA for p53 were expressed in the leading edge of migrating epithelium, with apoptosis patterns closely following those of p53 production. p53 mRNA levels decreased soon after wounding, but after a few days, levels increased to greater than baseline. bcl-2 was localized to the wound epithelium, but relative amounts tended to oppose levels of p53, i.e, when p53 increased, bcl-2 decreased and vice versa. |
| 105 | 10760214 | Wounds in diabetic animals showed a delayed onset of p53 mRNA expression but had persistently greater levels for longer periods of time. bcl-2 mRNA expression was further delayed in diabetic mice and did not develop to levels as high as p53. |
| 106 | 10760214 | Our data show that immediately after wounding, bcl-2 increases and p53 decreases to allow for the cellular proliferation that is required for tissue repair. |
| 107 | 10760214 | Over time, bcl-2 levels decrease while p53 levels increase to shut down the inflammatory process and down-regulate the proliferative response. |
| 108 | 10760214 | Diabetic animals appear to lose the indirect relationship between p53 and bcl-2. |
| 109 | 10760214 | Expression and localization of p53 and bcl-2 in healing wounds in diabetic and nondiabetic mice. |
| 110 | 10760214 | Another protein, bcl-2, is antagonistic to p53 and prevents apoptosis. |
| 111 | 10760214 | The purpose of this study was to determine the expression and location of p53 and bcl-2 mRNA and protein in healing wounds of normal and genetically diabetic mice. |
| 112 | 10760214 | At various time points, full-thickness skin wounds from nondiabetic and diabetic mice were evaluated for p53 and bcl-2 by immunohistochemistry and in situ hybridization. |
| 113 | 10760214 | Messenger RNA for p53 and bcl-2 were quantitated by competitive reverse transcriptase-polymerase chain reaction. |
| 114 | 10760214 | Protein and mRNA for p53 were expressed in the leading edge of migrating epithelium, with apoptosis patterns closely following those of p53 production. p53 mRNA levels decreased soon after wounding, but after a few days, levels increased to greater than baseline. bcl-2 was localized to the wound epithelium, but relative amounts tended to oppose levels of p53, i.e, when p53 increased, bcl-2 decreased and vice versa. |
| 115 | 10760214 | Wounds in diabetic animals showed a delayed onset of p53 mRNA expression but had persistently greater levels for longer periods of time. bcl-2 mRNA expression was further delayed in diabetic mice and did not develop to levels as high as p53. |
| 116 | 10760214 | Our data show that immediately after wounding, bcl-2 increases and p53 decreases to allow for the cellular proliferation that is required for tissue repair. |
| 117 | 10760214 | Over time, bcl-2 levels decrease while p53 levels increase to shut down the inflammatory process and down-regulate the proliferative response. |
| 118 | 10760214 | Diabetic animals appear to lose the indirect relationship between p53 and bcl-2. |
| 119 | 10760214 | Expression and localization of p53 and bcl-2 in healing wounds in diabetic and nondiabetic mice. |
| 120 | 10760214 | Another protein, bcl-2, is antagonistic to p53 and prevents apoptosis. |
| 121 | 10760214 | The purpose of this study was to determine the expression and location of p53 and bcl-2 mRNA and protein in healing wounds of normal and genetically diabetic mice. |
| 122 | 10760214 | At various time points, full-thickness skin wounds from nondiabetic and diabetic mice were evaluated for p53 and bcl-2 by immunohistochemistry and in situ hybridization. |
| 123 | 10760214 | Messenger RNA for p53 and bcl-2 were quantitated by competitive reverse transcriptase-polymerase chain reaction. |
| 124 | 10760214 | Protein and mRNA for p53 were expressed in the leading edge of migrating epithelium, with apoptosis patterns closely following those of p53 production. p53 mRNA levels decreased soon after wounding, but after a few days, levels increased to greater than baseline. bcl-2 was localized to the wound epithelium, but relative amounts tended to oppose levels of p53, i.e, when p53 increased, bcl-2 decreased and vice versa. |
| 125 | 10760214 | Wounds in diabetic animals showed a delayed onset of p53 mRNA expression but had persistently greater levels for longer periods of time. bcl-2 mRNA expression was further delayed in diabetic mice and did not develop to levels as high as p53. |
| 126 | 10760214 | Our data show that immediately after wounding, bcl-2 increases and p53 decreases to allow for the cellular proliferation that is required for tissue repair. |
| 127 | 10760214 | Over time, bcl-2 levels decrease while p53 levels increase to shut down the inflammatory process and down-regulate the proliferative response. |
| 128 | 10760214 | Diabetic animals appear to lose the indirect relationship between p53 and bcl-2. |
| 129 | 10760214 | Expression and localization of p53 and bcl-2 in healing wounds in diabetic and nondiabetic mice. |
| 130 | 10760214 | Another protein, bcl-2, is antagonistic to p53 and prevents apoptosis. |
| 131 | 10760214 | The purpose of this study was to determine the expression and location of p53 and bcl-2 mRNA and protein in healing wounds of normal and genetically diabetic mice. |
| 132 | 10760214 | At various time points, full-thickness skin wounds from nondiabetic and diabetic mice were evaluated for p53 and bcl-2 by immunohistochemistry and in situ hybridization. |
| 133 | 10760214 | Messenger RNA for p53 and bcl-2 were quantitated by competitive reverse transcriptase-polymerase chain reaction. |
| 134 | 10760214 | Protein and mRNA for p53 were expressed in the leading edge of migrating epithelium, with apoptosis patterns closely following those of p53 production. p53 mRNA levels decreased soon after wounding, but after a few days, levels increased to greater than baseline. bcl-2 was localized to the wound epithelium, but relative amounts tended to oppose levels of p53, i.e, when p53 increased, bcl-2 decreased and vice versa. |
| 135 | 10760214 | Wounds in diabetic animals showed a delayed onset of p53 mRNA expression but had persistently greater levels for longer periods of time. bcl-2 mRNA expression was further delayed in diabetic mice and did not develop to levels as high as p53. |
| 136 | 10760214 | Our data show that immediately after wounding, bcl-2 increases and p53 decreases to allow for the cellular proliferation that is required for tissue repair. |
| 137 | 10760214 | Over time, bcl-2 levels decrease while p53 levels increase to shut down the inflammatory process and down-regulate the proliferative response. |
| 138 | 10760214 | Diabetic animals appear to lose the indirect relationship between p53 and bcl-2. |
| 139 | 10760214 | Expression and localization of p53 and bcl-2 in healing wounds in diabetic and nondiabetic mice. |
| 140 | 10760214 | Another protein, bcl-2, is antagonistic to p53 and prevents apoptosis. |
| 141 | 10760214 | The purpose of this study was to determine the expression and location of p53 and bcl-2 mRNA and protein in healing wounds of normal and genetically diabetic mice. |
| 142 | 10760214 | At various time points, full-thickness skin wounds from nondiabetic and diabetic mice were evaluated for p53 and bcl-2 by immunohistochemistry and in situ hybridization. |
| 143 | 10760214 | Messenger RNA for p53 and bcl-2 were quantitated by competitive reverse transcriptase-polymerase chain reaction. |
| 144 | 10760214 | Protein and mRNA for p53 were expressed in the leading edge of migrating epithelium, with apoptosis patterns closely following those of p53 production. p53 mRNA levels decreased soon after wounding, but after a few days, levels increased to greater than baseline. bcl-2 was localized to the wound epithelium, but relative amounts tended to oppose levels of p53, i.e, when p53 increased, bcl-2 decreased and vice versa. |
| 145 | 10760214 | Wounds in diabetic animals showed a delayed onset of p53 mRNA expression but had persistently greater levels for longer periods of time. bcl-2 mRNA expression was further delayed in diabetic mice and did not develop to levels as high as p53. |
| 146 | 10760214 | Our data show that immediately after wounding, bcl-2 increases and p53 decreases to allow for the cellular proliferation that is required for tissue repair. |
| 147 | 10760214 | Over time, bcl-2 levels decrease while p53 levels increase to shut down the inflammatory process and down-regulate the proliferative response. |
| 148 | 10760214 | Diabetic animals appear to lose the indirect relationship between p53 and bcl-2. |
| 149 | 10760214 | Expression and localization of p53 and bcl-2 in healing wounds in diabetic and nondiabetic mice. |
| 150 | 10760214 | Another protein, bcl-2, is antagonistic to p53 and prevents apoptosis. |
| 151 | 10760214 | The purpose of this study was to determine the expression and location of p53 and bcl-2 mRNA and protein in healing wounds of normal and genetically diabetic mice. |
| 152 | 10760214 | At various time points, full-thickness skin wounds from nondiabetic and diabetic mice were evaluated for p53 and bcl-2 by immunohistochemistry and in situ hybridization. |
| 153 | 10760214 | Messenger RNA for p53 and bcl-2 were quantitated by competitive reverse transcriptase-polymerase chain reaction. |
| 154 | 10760214 | Protein and mRNA for p53 were expressed in the leading edge of migrating epithelium, with apoptosis patterns closely following those of p53 production. p53 mRNA levels decreased soon after wounding, but after a few days, levels increased to greater than baseline. bcl-2 was localized to the wound epithelium, but relative amounts tended to oppose levels of p53, i.e, when p53 increased, bcl-2 decreased and vice versa. |
| 155 | 10760214 | Wounds in diabetic animals showed a delayed onset of p53 mRNA expression but had persistently greater levels for longer periods of time. bcl-2 mRNA expression was further delayed in diabetic mice and did not develop to levels as high as p53. |
| 156 | 10760214 | Our data show that immediately after wounding, bcl-2 increases and p53 decreases to allow for the cellular proliferation that is required for tissue repair. |
| 157 | 10760214 | Over time, bcl-2 levels decrease while p53 levels increase to shut down the inflammatory process and down-regulate the proliferative response. |
| 158 | 10760214 | Diabetic animals appear to lose the indirect relationship between p53 and bcl-2. |
| 159 | 10760214 | Expression and localization of p53 and bcl-2 in healing wounds in diabetic and nondiabetic mice. |
| 160 | 10760214 | Another protein, bcl-2, is antagonistic to p53 and prevents apoptosis. |
| 161 | 10760214 | The purpose of this study was to determine the expression and location of p53 and bcl-2 mRNA and protein in healing wounds of normal and genetically diabetic mice. |
| 162 | 10760214 | At various time points, full-thickness skin wounds from nondiabetic and diabetic mice were evaluated for p53 and bcl-2 by immunohistochemistry and in situ hybridization. |
| 163 | 10760214 | Messenger RNA for p53 and bcl-2 were quantitated by competitive reverse transcriptase-polymerase chain reaction. |
| 164 | 10760214 | Protein and mRNA for p53 were expressed in the leading edge of migrating epithelium, with apoptosis patterns closely following those of p53 production. p53 mRNA levels decreased soon after wounding, but after a few days, levels increased to greater than baseline. bcl-2 was localized to the wound epithelium, but relative amounts tended to oppose levels of p53, i.e, when p53 increased, bcl-2 decreased and vice versa. |
| 165 | 10760214 | Wounds in diabetic animals showed a delayed onset of p53 mRNA expression but had persistently greater levels for longer periods of time. bcl-2 mRNA expression was further delayed in diabetic mice and did not develop to levels as high as p53. |
| 166 | 10760214 | Our data show that immediately after wounding, bcl-2 increases and p53 decreases to allow for the cellular proliferation that is required for tissue repair. |
| 167 | 10760214 | Over time, bcl-2 levels decrease while p53 levels increase to shut down the inflammatory process and down-regulate the proliferative response. |
| 168 | 10760214 | Diabetic animals appear to lose the indirect relationship between p53 and bcl-2. |
| 169 | 10760214 | Expression and localization of p53 and bcl-2 in healing wounds in diabetic and nondiabetic mice. |
| 170 | 10760214 | Another protein, bcl-2, is antagonistic to p53 and prevents apoptosis. |
| 171 | 10760214 | The purpose of this study was to determine the expression and location of p53 and bcl-2 mRNA and protein in healing wounds of normal and genetically diabetic mice. |
| 172 | 10760214 | At various time points, full-thickness skin wounds from nondiabetic and diabetic mice were evaluated for p53 and bcl-2 by immunohistochemistry and in situ hybridization. |
| 173 | 10760214 | Messenger RNA for p53 and bcl-2 were quantitated by competitive reverse transcriptase-polymerase chain reaction. |
| 174 | 10760214 | Protein and mRNA for p53 were expressed in the leading edge of migrating epithelium, with apoptosis patterns closely following those of p53 production. p53 mRNA levels decreased soon after wounding, but after a few days, levels increased to greater than baseline. bcl-2 was localized to the wound epithelium, but relative amounts tended to oppose levels of p53, i.e, when p53 increased, bcl-2 decreased and vice versa. |
| 175 | 10760214 | Wounds in diabetic animals showed a delayed onset of p53 mRNA expression but had persistently greater levels for longer periods of time. bcl-2 mRNA expression was further delayed in diabetic mice and did not develop to levels as high as p53. |
| 176 | 10760214 | Our data show that immediately after wounding, bcl-2 increases and p53 decreases to allow for the cellular proliferation that is required for tissue repair. |
| 177 | 10760214 | Over time, bcl-2 levels decrease while p53 levels increase to shut down the inflammatory process and down-regulate the proliferative response. |
| 178 | 10760214 | Diabetic animals appear to lose the indirect relationship between p53 and bcl-2. |
| 179 | 10830283 | Cytokines induce both necrosis and apoptosis via a common Bcl-2-inhibitable pathway in rat insulin-producing cells. |
| 180 | 10830283 | A combination of interleukin-1beta, interferon-gamma, and tumor necrosis factor-alpha increased both necrosis (17% of cells) and apoptosis (5% of cells) in isolated whole rat islets, as determined by vital staining and fluorescence microscopy. |
| 181 | 10830283 | Hyperexpression of Bcl-2, achieved by stable transfection using a multicopy viral vector containing a bcl-2 complementary DNA in rat insulin-producing RINm5F cells, counteracted both apoptosis and necrosis. |
| 182 | 10830283 | Cytokine-induced cleavage of the caspase-3 substrate poly(ADP-ribose) polymerase (which, in other cell types, may occur downstream or independently of a Bcl-2-preventable mitochondrial permeability transition) was observed in control- but neither in bcl-2-transfected cells nor in the presence of the iNOS inhibitor N(G)-methyl-L-arginine. |
| 183 | 10830283 | Tumor necrosis factor-alpha alone did not clearly induce cell death or poly(ADP-ribose) polymerase-cleavage. |
| 184 | 10830283 | These findings suggest that cytokines induce both necrosis and apoptosis in insulin-producing cells via a common Bcl-2-preventable nitric oxide-dependent pathway, which may involve mitochondrial permeability transition. |
| 185 | 10830283 | Cytokines induce both necrosis and apoptosis via a common Bcl-2-inhibitable pathway in rat insulin-producing cells. |
| 186 | 10830283 | A combination of interleukin-1beta, interferon-gamma, and tumor necrosis factor-alpha increased both necrosis (17% of cells) and apoptosis (5% of cells) in isolated whole rat islets, as determined by vital staining and fluorescence microscopy. |
| 187 | 10830283 | Hyperexpression of Bcl-2, achieved by stable transfection using a multicopy viral vector containing a bcl-2 complementary DNA in rat insulin-producing RINm5F cells, counteracted both apoptosis and necrosis. |
| 188 | 10830283 | Cytokine-induced cleavage of the caspase-3 substrate poly(ADP-ribose) polymerase (which, in other cell types, may occur downstream or independently of a Bcl-2-preventable mitochondrial permeability transition) was observed in control- but neither in bcl-2-transfected cells nor in the presence of the iNOS inhibitor N(G)-methyl-L-arginine. |
| 189 | 10830283 | Tumor necrosis factor-alpha alone did not clearly induce cell death or poly(ADP-ribose) polymerase-cleavage. |
| 190 | 10830283 | These findings suggest that cytokines induce both necrosis and apoptosis in insulin-producing cells via a common Bcl-2-preventable nitric oxide-dependent pathway, which may involve mitochondrial permeability transition. |
| 191 | 10830283 | Cytokines induce both necrosis and apoptosis via a common Bcl-2-inhibitable pathway in rat insulin-producing cells. |
| 192 | 10830283 | A combination of interleukin-1beta, interferon-gamma, and tumor necrosis factor-alpha increased both necrosis (17% of cells) and apoptosis (5% of cells) in isolated whole rat islets, as determined by vital staining and fluorescence microscopy. |
| 193 | 10830283 | Hyperexpression of Bcl-2, achieved by stable transfection using a multicopy viral vector containing a bcl-2 complementary DNA in rat insulin-producing RINm5F cells, counteracted both apoptosis and necrosis. |
| 194 | 10830283 | Cytokine-induced cleavage of the caspase-3 substrate poly(ADP-ribose) polymerase (which, in other cell types, may occur downstream or independently of a Bcl-2-preventable mitochondrial permeability transition) was observed in control- but neither in bcl-2-transfected cells nor in the presence of the iNOS inhibitor N(G)-methyl-L-arginine. |
| 195 | 10830283 | Tumor necrosis factor-alpha alone did not clearly induce cell death or poly(ADP-ribose) polymerase-cleavage. |
| 196 | 10830283 | These findings suggest that cytokines induce both necrosis and apoptosis in insulin-producing cells via a common Bcl-2-preventable nitric oxide-dependent pathway, which may involve mitochondrial permeability transition. |
| 197 | 10830283 | Cytokines induce both necrosis and apoptosis via a common Bcl-2-inhibitable pathway in rat insulin-producing cells. |
| 198 | 10830283 | A combination of interleukin-1beta, interferon-gamma, and tumor necrosis factor-alpha increased both necrosis (17% of cells) and apoptosis (5% of cells) in isolated whole rat islets, as determined by vital staining and fluorescence microscopy. |
| 199 | 10830283 | Hyperexpression of Bcl-2, achieved by stable transfection using a multicopy viral vector containing a bcl-2 complementary DNA in rat insulin-producing RINm5F cells, counteracted both apoptosis and necrosis. |
| 200 | 10830283 | Cytokine-induced cleavage of the caspase-3 substrate poly(ADP-ribose) polymerase (which, in other cell types, may occur downstream or independently of a Bcl-2-preventable mitochondrial permeability transition) was observed in control- but neither in bcl-2-transfected cells nor in the presence of the iNOS inhibitor N(G)-methyl-L-arginine. |
| 201 | 10830283 | Tumor necrosis factor-alpha alone did not clearly induce cell death or poly(ADP-ribose) polymerase-cleavage. |
| 202 | 10830283 | These findings suggest that cytokines induce both necrosis and apoptosis in insulin-producing cells via a common Bcl-2-preventable nitric oxide-dependent pathway, which may involve mitochondrial permeability transition. |
| 203 | 10843893 | Glucose treatment also mediated an upregulation of the cardioprotective factor Bcl-2 but did not affect the cellular content of the proapoptotic factors Bax and Bad. |
| 204 | 10851311 | Loss of TGFbeta, Apoptosis, and Bcl-2 in Erectile Dysfunction and Upregulation of p53 and HIF-1alpha in Diabetes-Associated Erectile Dysfunction. |
| 205 | 10851311 | Vasculogenic erectile dysfunction (ED) is associated with collagen replacement of the cavernosal smooth muscle, mediated by an increase in transforming growth factor (TGF)-production secondary to hypoxemia. |
| 206 | 10851311 | We tested the hypothesis that human ED is the result of an increase in apoptosis of the cavernosal smooth muscle cells with replacement by collagen, mediated by the TGFbeta upregulation. |
| 207 | 10851311 | Immunohistochemistry staining was used to detect TGFbeta and Bcl-2 expression, while Western blot analysis was used to detect expression of Bcl-2, p53, and hypoxia-inducible factor (HIF)-1a. |
| 208 | 10851311 | In contrast, Western blotting demonstrated upregulation of p53 and HIF-1a expression in the cavernosal tissues from the men with ED and diabetes. |
| 209 | 10851311 | Male ED follows an active process characterized by a loss of TGFb expression, apoptosis, and Bcl-2 expression. |
| 210 | 10851311 | However, there is upregulation of p53 and HIF-1a in men with diabetes. |
| 211 | 10851311 | These data support the possibility of hypoxia-mediated ED in diabetes via upregulation of p53 and HIF-1a but does not substantiate a role for TGFbeta in ED. |
| 212 | 10851311 | Loss of TGFbeta, Apoptosis, and Bcl-2 in Erectile Dysfunction and Upregulation of p53 and HIF-1alpha in Diabetes-Associated Erectile Dysfunction. |
| 213 | 10851311 | Vasculogenic erectile dysfunction (ED) is associated with collagen replacement of the cavernosal smooth muscle, mediated by an increase in transforming growth factor (TGF)-production secondary to hypoxemia. |
| 214 | 10851311 | We tested the hypothesis that human ED is the result of an increase in apoptosis of the cavernosal smooth muscle cells with replacement by collagen, mediated by the TGFbeta upregulation. |
| 215 | 10851311 | Immunohistochemistry staining was used to detect TGFbeta and Bcl-2 expression, while Western blot analysis was used to detect expression of Bcl-2, p53, and hypoxia-inducible factor (HIF)-1a. |
| 216 | 10851311 | In contrast, Western blotting demonstrated upregulation of p53 and HIF-1a expression in the cavernosal tissues from the men with ED and diabetes. |
| 217 | 10851311 | Male ED follows an active process characterized by a loss of TGFb expression, apoptosis, and Bcl-2 expression. |
| 218 | 10851311 | However, there is upregulation of p53 and HIF-1a in men with diabetes. |
| 219 | 10851311 | These data support the possibility of hypoxia-mediated ED in diabetes via upregulation of p53 and HIF-1a but does not substantiate a role for TGFbeta in ED. |
| 220 | 10851311 | Loss of TGFbeta, Apoptosis, and Bcl-2 in Erectile Dysfunction and Upregulation of p53 and HIF-1alpha in Diabetes-Associated Erectile Dysfunction. |
| 221 | 10851311 | Vasculogenic erectile dysfunction (ED) is associated with collagen replacement of the cavernosal smooth muscle, mediated by an increase in transforming growth factor (TGF)-production secondary to hypoxemia. |
| 222 | 10851311 | We tested the hypothesis that human ED is the result of an increase in apoptosis of the cavernosal smooth muscle cells with replacement by collagen, mediated by the TGFbeta upregulation. |
| 223 | 10851311 | Immunohistochemistry staining was used to detect TGFbeta and Bcl-2 expression, while Western blot analysis was used to detect expression of Bcl-2, p53, and hypoxia-inducible factor (HIF)-1a. |
| 224 | 10851311 | In contrast, Western blotting demonstrated upregulation of p53 and HIF-1a expression in the cavernosal tissues from the men with ED and diabetes. |
| 225 | 10851311 | Male ED follows an active process characterized by a loss of TGFb expression, apoptosis, and Bcl-2 expression. |
| 226 | 10851311 | However, there is upregulation of p53 and HIF-1a in men with diabetes. |
| 227 | 10851311 | These data support the possibility of hypoxia-mediated ED in diabetes via upregulation of p53 and HIF-1a but does not substantiate a role for TGFbeta in ED. |
| 228 | 11000281 | Apoptosis and occurrence of Bcl-2, Bak, Bax, Fas and FasL in the developing and adult rat endocrine pancreas. |
| 229 | 11000281 | At each time point, histologic sections were treated with the direct fluorescein-labelled TUNEL method and immunostained for pancreatic hormones (glucagon, insulin), apoptotic promoters (Bak, Bax, Fas, Fas Ligand) as well as for the anti-apoptotic peptide Bcl-2. |
| 230 | 11000281 | The first phase began at E19 and peaked at P5 accompanied by a considerable increase in Bak fluorescence staining intensity, while the second phase began at P30 and peaked at 18 months with increasing amounts of Fas and FasL staining intensities in the islet cells. |
| 231 | 11000281 | Apoptosis and occurrence of Bcl-2, Bak, Bax, Fas and FasL in the developing and adult rat endocrine pancreas. |
| 232 | 11000281 | At each time point, histologic sections were treated with the direct fluorescein-labelled TUNEL method and immunostained for pancreatic hormones (glucagon, insulin), apoptotic promoters (Bak, Bax, Fas, Fas Ligand) as well as for the anti-apoptotic peptide Bcl-2. |
| 233 | 11000281 | The first phase began at E19 and peaked at P5 accompanied by a considerable increase in Bak fluorescence staining intensity, while the second phase began at P30 and peaked at 18 months with increasing amounts of Fas and FasL staining intensities in the islet cells. |
| 234 | 11016460 | NOD Idd5 locus controls insulitis and diabetes and overlaps the orthologous CTLA4/IDDM12 and NRAMP1 loci in humans. |
| 235 | 11016460 | This locus was designated Idd5 and encompassed candidate genes including Il1r1, Il1r2, Stat1, Stat4, Nramp1, and Bcl2. |
| 236 | 11016460 | Idd5.1 is in the proximal 1.5-cM portion of the interval and contains the candidates Casp8, Cflar (FLIP), Cd28, and Cd152 (CTLA4). |
| 237 | 11016460 | Idd5.2 is in the distal 5.1-cM portion of the 9.4-cM interval and contains the candidates Nramp1, which has a functional polymorphism between NOD and B10, and Cmkar2 (CXCR2, interleukin [IL]-8 receptor alpha). |
| 238 | 11016460 | Candidate genes eliminated by this analysis include Il1r1, Ilr2, Zap70, Orch5, Stat1, Stat4, Bcl2, Cmkar4 (CXCR4), and Il10. |
| 239 | 11016460 | NOD Idd5 locus controls insulitis and diabetes and overlaps the orthologous CTLA4/IDDM12 and NRAMP1 loci in humans. |
| 240 | 11016460 | This locus was designated Idd5 and encompassed candidate genes including Il1r1, Il1r2, Stat1, Stat4, Nramp1, and Bcl2. |
| 241 | 11016460 | Idd5.1 is in the proximal 1.5-cM portion of the interval and contains the candidates Casp8, Cflar (FLIP), Cd28, and Cd152 (CTLA4). |
| 242 | 11016460 | Idd5.2 is in the distal 5.1-cM portion of the 9.4-cM interval and contains the candidates Nramp1, which has a functional polymorphism between NOD and B10, and Cmkar2 (CXCR2, interleukin [IL]-8 receptor alpha). |
| 243 | 11016460 | Candidate genes eliminated by this analysis include Il1r1, Ilr2, Zap70, Orch5, Stat1, Stat4, Bcl2, Cmkar4 (CXCR4), and Il10. |
| 244 | 11044408 | Bcl-x is a member of the Bcl2 family and has been suggested to be important for the survival and maturation of various cell types including the erythroid lineage. |
| 245 | 11044408 | The increase in cell death of late erythroid cells is independent from the proapoptotic factor Bax, as demonstrated in conditional double mutant mice for Bcl-x and Bax. |
| 246 | 11078462 | Intact and acutely dissociated neurons from diabetic rats demonstrated decreased Bcl-2 levels and translocation of cytochrome C from the mitochondria to the cytoplasm. |
| 247 | 11078462 | Neither levels of Bax nor levels of Bcl-XL were altered in diabetic neuropathy. |
| 248 | 11090239 | Cell proliferation nuclear antigen (PCNA) was used as a marker of cell proliferation and cells were stained for putative markers of islet neogenesis, cytokeratin 20 (CK20) and Bcl-2. |
| 249 | 11090239 | Most of the insulin(+)clusters were also homeodomain-containing transcription factor pancreas duodenum homeobox gene-1 (PDX-1) positive. |
| 250 | 11126237 | The levels of the cell survival proteins Bcl-2 and neuronal apoptosis inhibitory protein (NAIP) have been observed to increase during adipogenesis. |
| 251 | 11375329 | The antiapoptotic gene Bcl-2 was unaffected by glucose change, whereas Bcl-xl was reduced upon treatment with HG5. |
| 252 | 11375329 | On the other hand, proapoptotic genes Bad, Bid, and Bik were overexpressed in the islets maintained in HG5. |
| 253 | 11375329 | Bik and Bcl-xl were expressed in other endocrine islet cells as well as in the exocrine pancreas. |
| 254 | 11561209 | Herein, a focal point is the mitochondrial control of specific death enzymes--so called caspases--by members of the pro-apoptotic Bax and BH3 subfamily or the anti-apoptotic Bcl-2 subfamily. |
| 255 | 11561209 | The insulin-like growth factors (IGFs) are potent proliferation factors and potently inhibit apoptosis acting via the ubiquitously expressed IGF-I receptor. |
| 256 | 11561209 | Within IGF-I receptor signalling, key to the inhibition of apoptosis are the RAS/RAF/mitogen-activated protein (MAP)-kinase pathway and the PI 3'-kinase pathway. |
| 257 | 11563854 | Stimulation of HAECs with gly-ox-HDL elicited a marked increase in caspase 3 activity and the expressions of active caspase 3 and caspase 9, whereas concomitant treatment with a caspase 3 inhibitor significantly blocked gly-ox-HDL-induced apoptosis of HAECs. |
| 258 | 11563854 | The increased expressions of Bax and Bad were detected in HAECs incubated for 24 h with gly-ox-HDL, but gly-ox-HDL failed to interfere with the expression of Bcl-2 and Bcl-x. |
| 259 | 11731240 | In the mammary gland Bcl-x is the most abundant cell survival factor from the Bcl-2 family. |
| 260 | 11731240 | In erythroid cells bcl-x gene expression is controlled by cytokines and the transcription factor Stat5 (signal transducer and activator of transcription). |
| 261 | 11731240 | However, we identified that bcl-x RNA levels in mammary tissue from prolactin receptor- and Stat5-null mice were indistinguishable from wild type mice. |
| 262 | 11751624 | Exposure of rat beta-cells to the combination of IL-1beta plus interferon-gamma causes a time-dependent increase in apoptotic cells starting after 3 d (<10% on d 3 and 28 +/- 2% on d 7). |
| 263 | 11751624 | This effect was preceded by a marked down-regulation of two antiapoptotic proteins, Bcl-2 and Bax-omega (respectively reduced by 60% and 80% after 3 d), whereas no changes occurred in the expression of Bcl-x(L) and the proapoptotic protein Bax-alpha. |
| 264 | 11751624 | No apoptosis or down-regulation of Bcl-2 and Bax-omega proteins was observed with individual cytokines or in the presence of N-methyl-L-arginine, an inhibitor of nitric oxide synthase. |
| 265 | 11751624 | Exposure of rat beta-cells to the combination of IL-1beta plus interferon-gamma causes a time-dependent increase in apoptotic cells starting after 3 d (<10% on d 3 and 28 +/- 2% on d 7). |
| 266 | 11751624 | This effect was preceded by a marked down-regulation of two antiapoptotic proteins, Bcl-2 and Bax-omega (respectively reduced by 60% and 80% after 3 d), whereas no changes occurred in the expression of Bcl-x(L) and the proapoptotic protein Bax-alpha. |
| 267 | 11751624 | No apoptosis or down-regulation of Bcl-2 and Bax-omega proteins was observed with individual cytokines or in the presence of N-methyl-L-arginine, an inhibitor of nitric oxide synthase. |
| 268 | 11797699 | Results obtained utilizing a variety of NMR techniques demonstrate the following: (1) Transfection of Rat1 cells with the c-myc oncogene (which may be involved in cell proliferation and cell cycle regulation) and overexpression of Bcl-2 (which may protect cells from stresses such as hypoxia and exposure to cytokines) introduce a wide array of alterations in cellular biochemistry, including changes in anaerobic and oxidative glucose metabolism, as assessed by 13C and 31P NMR spectroscopy. (2) Overnight incubation of islets and beta cells in the bottom of centrifuge tubes filled with medium at room temperature, as is sometimes done in islet transportation, exposes them to severe oxygen limitations that may cause cell damage. |
| 269 | 11812749 | A variety of protective genes were upregulated, with markedly increased expression of the antioxidant genes heme oxygenase-1 and glutathione peroxidase and the antiapoptotic gene A20. |
| 270 | 11812749 | Cu/Zn-superoxide dismutase (SOD) and Mn-SOD were modestly induced, and Bcl-2 was modestly reduced; however, several other stress genes (catalase, heat shock protein 70, and p53) were unaltered. |
| 271 | 11813268 | After 72 h exposure of human pancreatic islets to a cytotoxic cytokine combination of interleukin 1 beta (50 U/ml), tumor necrosis factor alpha (1,000 U/ml), and interferon gamma (1,000 U/ml), an increase of cell death vs. control islets was demonstrated by TUNEL and cell death detection ELISA method. |
| 272 | 11813268 | This effect was correlated with a marked decrease of Bcl-2 mRNA expression (without any major change of Bax mRNA) and a marked increase of inducible nitric oxide synthase mRNA. |
| 273 | 11899074 | The delivery of transgenes capable of interfering with antigenic recognition and/or cell death [e.g., Fas ligand (FasL), Bcl-2, Bcl-XL] as well as imparting tolerance/immunoregulation [e.g., interleukin(IL)-4, IL-10, transforming growth factor (TGF)-beta], or cytoprotection [e.g., heme oxygenase-1 (HO-1), catalase, manganese superoxide dismutase (MnSOD)] may prevent recurrent type 1 diabetes in islet transplantation and offer a promising form of immunotherapy. |
| 274 | 11978640 | RT-PCR studies revealed no major change of iNOS and Bax mRNA expression and a marked decrease of Bcl-2 mRNA expression in the islets cultured with FFA. |
| 275 | 12145177 | High D-glucose significantly increased bax protein, but not bcl-2, and activated caspase 3-like and 9, whereas HGF significantly increased bcl-2 expression without affecting bax level and attenuated the increase in caspase 3 and 9 activity. |
| 276 | 12145177 | Interestingly, high D-glucose resulted in translocation of bax protein from cytosol to the mitochondrial membrane, whereas HGF inhibited the bax translocation. |
| 277 | 12145177 | These findings suggest that HGF can activate bcl-2 expression and inhibit translocation of bax protein upstream of the mitochondria, thereby leading to the inhibition of caspase 3 and 9 activation. |
| 278 | 12145177 | High D-glucose significantly increased bax protein, but not bcl-2, and activated caspase 3-like and 9, whereas HGF significantly increased bcl-2 expression without affecting bax level and attenuated the increase in caspase 3 and 9 activity. |
| 279 | 12145177 | Interestingly, high D-glucose resulted in translocation of bax protein from cytosol to the mitochondrial membrane, whereas HGF inhibited the bax translocation. |
| 280 | 12145177 | These findings suggest that HGF can activate bcl-2 expression and inhibit translocation of bax protein upstream of the mitochondria, thereby leading to the inhibition of caspase 3 and 9 activation. |
| 281 | 12164338 | Apoptosis in normal rat embryo tissues during early organogenesis: the possible involvement of Bax and Bcl-2. |
| 282 | 12164338 | In this study, we investigated the relationship between apoptosis and the expression of both Bax and Bcl-2 during the early organogenesis period (9.5-11.5 days of gestation) of rat embryos. |
| 283 | 12164338 | Immunohistochemical studies of Bax and Bcl-2 expression revealed that these apoptotic cells were exactly positive to Bax in mirror sections, while their expression of Bcl-2 was generally too low to be detected. |
| 284 | 12164338 | These results indicate that the Bax and Bcl-2 may be important in regulating the induction of embryonic cell apoptosis during early organogenesis. |
| 285 | 12164338 | Apoptosis in normal rat embryo tissues during early organogenesis: the possible involvement of Bax and Bcl-2. |
| 286 | 12164338 | In this study, we investigated the relationship between apoptosis and the expression of both Bax and Bcl-2 during the early organogenesis period (9.5-11.5 days of gestation) of rat embryos. |
| 287 | 12164338 | Immunohistochemical studies of Bax and Bcl-2 expression revealed that these apoptotic cells were exactly positive to Bax in mirror sections, while their expression of Bcl-2 was generally too low to be detected. |
| 288 | 12164338 | These results indicate that the Bax and Bcl-2 may be important in regulating the induction of embryonic cell apoptosis during early organogenesis. |
| 289 | 12164338 | Apoptosis in normal rat embryo tissues during early organogenesis: the possible involvement of Bax and Bcl-2. |
| 290 | 12164338 | In this study, we investigated the relationship between apoptosis and the expression of both Bax and Bcl-2 during the early organogenesis period (9.5-11.5 days of gestation) of rat embryos. |
| 291 | 12164338 | Immunohistochemical studies of Bax and Bcl-2 expression revealed that these apoptotic cells were exactly positive to Bax in mirror sections, while their expression of Bcl-2 was generally too low to be detected. |
| 292 | 12164338 | These results indicate that the Bax and Bcl-2 may be important in regulating the induction of embryonic cell apoptosis during early organogenesis. |
| 293 | 12164338 | Apoptosis in normal rat embryo tissues during early organogenesis: the possible involvement of Bax and Bcl-2. |
| 294 | 12164338 | In this study, we investigated the relationship between apoptosis and the expression of both Bax and Bcl-2 during the early organogenesis period (9.5-11.5 days of gestation) of rat embryos. |
| 295 | 12164338 | Immunohistochemical studies of Bax and Bcl-2 expression revealed that these apoptotic cells were exactly positive to Bax in mirror sections, while their expression of Bcl-2 was generally too low to be detected. |
| 296 | 12164338 | These results indicate that the Bax and Bcl-2 may be important in regulating the induction of embryonic cell apoptosis during early organogenesis. |
| 297 | 12200129 | Pigment epithelium-derived factor (PEDF) has recently been shown to be the most potent inhibitor of angiogenesis in the mammalian eye, suggesting that loss of PEDF is involved in the pathogenesis of proliferative diabetic retinopathy. |
| 298 | 12200129 | Further, PEDF proteins completely restored the down-regulation of bcl-2 gene expression in AGE-exposed pericytes. |
| 299 | 12242483 | Immunohistochemically, small cells are positive for PDX-1, synaptophysin, insulin, glucagon, somatostatin, pancreatic polypeptide, alpha-fetaprotein and Bcl-2 and negative for cytokeratin 19 and nestin. |
| 300 | 12370856 | In islets cultured for 7 days in the presence of high FFA or for 3 days in the presence of high glucose levels, we observed: (1) a 2- to 3-fold increase of apoptotic cells conjugated with annexin-V FITC and PI; (2) a 4- to 6-fold increase of cytoplasmatic DNA fragments; (3) a 3- to 4-fold increase of caspase 3 activity; and (4) a significant increase of insulin positive apoptotic cells as detected with the TUNEL method. |
| 301 | 12370856 | RT-PCR analysis indicated in islets exposed to high FFA or glucose levels an increase of bax (proapoptotic gene), a reduction of bcl-2 (antiapoptotic gene), and a slight (although not significant) increase in caspase 3 expression. |
| 302 | 12533681 | By immunohistochemistry, we demonstrated increased expression of Fas, Fas ligand (FasL), and bcl-2 on SMG epithelial cells of NOD and NOD-scid mice, as early as 3 days of age. mRNA expression of Fas and FasL was also examined in SMG by RQ-PCR. |
| 303 | 12533681 | Low-level expression of Fas and FasL mRNA was observed in all mouse strains, from 1 day of age onward. |
| 304 | 12533681 | We conclude that increased protein expression of Fas and FasL on SMG epithelial cells of NOD and NOD-scid mice probably indicates a genetically programmed abnormality in these cells that may form a trigger for the development of sialoadenitis in NOD mice. |
| 305 | 12594237 | Therefore, we used early postnatal mouse pancreata from three control strains (C57BL/6, DBA/2, BALB/c) and from two strains with the nonobese diabetic (NOD)-related genetic background (the spontaneous T1D NOD model and the lymphocyte-deficient NODscid strain) to study apoptotic phenomena together with the molecular and immunohistochemical expression of proapoptosis (Fas, FasL) and antiapoptosis (Bcl-2) proteins. |
| 306 | 12594237 | Second, FasL(+), Fas(+), and Bcl-2(+) structures seemed to be associated with innervation, regardless of the strain and age. |
| 307 | 12594237 | Therefore, we used early postnatal mouse pancreata from three control strains (C57BL/6, DBA/2, BALB/c) and from two strains with the nonobese diabetic (NOD)-related genetic background (the spontaneous T1D NOD model and the lymphocyte-deficient NODscid strain) to study apoptotic phenomena together with the molecular and immunohistochemical expression of proapoptosis (Fas, FasL) and antiapoptosis (Bcl-2) proteins. |
| 308 | 12594237 | Second, FasL(+), Fas(+), and Bcl-2(+) structures seemed to be associated with innervation, regardless of the strain and age. |
| 309 | 12606514 | In addition, palmitic acid decreased Bcl-2 expression and induced release of cytochrome c from the mitochondria into the cytosol, which was prevented by fumonisin B1 and by oleic acid. |
| 310 | 12658358 | The immunohistochemistry and RT-PCR assay showed a higher level of Fas expression and Fas mRNA in the cataracts with DR than in the senile cataracts, although there was no difference in the expression level of the Fas ligand, Bcl-2, and their mRNAs between both groups. |
| 311 | 12663450 | The proapoptotic factor Nix is coexpressed with Bcl-xL during terminal erythroid differentiation. |
| 312 | 12663450 | Our in silico screening strategy indicated that a hypoxia-inducible proapoptotic member of the Bcl-2 gene family called Nix is expressed during erythropoiesis. |
| 313 | 12663450 | Polymerase chain reaction (PCR)-based transcriptional patterning confirmed the increased expression of Nix during human erythropoiesis with a pattern similar to that of Bcl-xL and glycophorin A and opposite that of Bcl-2. |
| 314 | 12663450 | The expression of Nix and Bcl-xL proteins decreased relative to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) control on the removal of erythropoietin (EPO) from the culture medium. |
| 315 | 12663450 | The proapoptotic factor Nix is coexpressed with Bcl-xL during terminal erythroid differentiation. |
| 316 | 12663450 | Our in silico screening strategy indicated that a hypoxia-inducible proapoptotic member of the Bcl-2 gene family called Nix is expressed during erythropoiesis. |
| 317 | 12663450 | Polymerase chain reaction (PCR)-based transcriptional patterning confirmed the increased expression of Nix during human erythropoiesis with a pattern similar to that of Bcl-xL and glycophorin A and opposite that of Bcl-2. |
| 318 | 12663450 | The expression of Nix and Bcl-xL proteins decreased relative to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) control on the removal of erythropoietin (EPO) from the culture medium. |
| 319 | 12697734 | Mice with 50% Pdx1, a homeobox gene critical for pancreatic development, had worsening glucose tolerance with age and reduced insulin release in response to glucose, KCl, and arginine from the perfused pancreas. |
| 320 | 12697734 | Surprisingly, insulin secretion in perifusion or static incubation experiments in response to glucose and other secretagogues was similar in islets isolated from Pdx1(+/-) mice compared with Pdx1(+/+) littermate controls. |
| 321 | 12697734 | Bcl(XL) and Bcl-2 expression were reduced in Pdx1(+/-) islets. |
| 322 | 12697734 | These results suggest that an increase in apoptosis, with abnormal regulation of islet number and beta cell mass, represents a key mechanism whereby partial PDX1 deficiency leads to an organ-level defect in insulin secretion and diabetes. |
| 323 | 12765953 | To this end, two strategies that have emerged for procuring cell lines with resistance to immune-mediated damage are 1) selection of cytokine-resistant cell lines by growth of INS-1 insulinoma cells in iteratively increasing concentrations of interleukin (IL)-1beta + gamma-interferon (IFN-gamma), and 2) stable overexpression of the anti-apoptotic gene bcl-2 in INS-1 cells. |
| 324 | 12765953 | Herein, we show that bcl-2-overexpressing cells are resistant to the cytotoxic effects of reactive oxygen and nitrogen species (ROS/RNS), but are only modestly protected against high concentrations of IL-1beta + INF-gamma, whereas the converse is true in cytokine selected cells. |
| 325 | 12765953 | We also found that the combination of bcl-2 expression and cytokine selection confers a broader spectrum of resistance than either procedure alone, such that the resultant cells are highly resistant to cytokines and ROS/RNS, with no impairment in glucose-stimulated insulin secretion. |
| 326 | 12765953 | INS-1-derived cells with combined bcl-2 expression and cytokine selection are also more resistant to damage induced by coculture with mitogen-activated peripheral blood mononuclear cells. |
| 327 | 12765953 | To this end, two strategies that have emerged for procuring cell lines with resistance to immune-mediated damage are 1) selection of cytokine-resistant cell lines by growth of INS-1 insulinoma cells in iteratively increasing concentrations of interleukin (IL)-1beta + gamma-interferon (IFN-gamma), and 2) stable overexpression of the anti-apoptotic gene bcl-2 in INS-1 cells. |
| 328 | 12765953 | Herein, we show that bcl-2-overexpressing cells are resistant to the cytotoxic effects of reactive oxygen and nitrogen species (ROS/RNS), but are only modestly protected against high concentrations of IL-1beta + INF-gamma, whereas the converse is true in cytokine selected cells. |
| 329 | 12765953 | We also found that the combination of bcl-2 expression and cytokine selection confers a broader spectrum of resistance than either procedure alone, such that the resultant cells are highly resistant to cytokines and ROS/RNS, with no impairment in glucose-stimulated insulin secretion. |
| 330 | 12765953 | INS-1-derived cells with combined bcl-2 expression and cytokine selection are also more resistant to damage induced by coculture with mitogen-activated peripheral blood mononuclear cells. |
| 331 | 12765953 | To this end, two strategies that have emerged for procuring cell lines with resistance to immune-mediated damage are 1) selection of cytokine-resistant cell lines by growth of INS-1 insulinoma cells in iteratively increasing concentrations of interleukin (IL)-1beta + gamma-interferon (IFN-gamma), and 2) stable overexpression of the anti-apoptotic gene bcl-2 in INS-1 cells. |
| 332 | 12765953 | Herein, we show that bcl-2-overexpressing cells are resistant to the cytotoxic effects of reactive oxygen and nitrogen species (ROS/RNS), but are only modestly protected against high concentrations of IL-1beta + INF-gamma, whereas the converse is true in cytokine selected cells. |
| 333 | 12765953 | We also found that the combination of bcl-2 expression and cytokine selection confers a broader spectrum of resistance than either procedure alone, such that the resultant cells are highly resistant to cytokines and ROS/RNS, with no impairment in glucose-stimulated insulin secretion. |
| 334 | 12765953 | INS-1-derived cells with combined bcl-2 expression and cytokine selection are also more resistant to damage induced by coculture with mitogen-activated peripheral blood mononuclear cells. |
| 335 | 12765953 | To this end, two strategies that have emerged for procuring cell lines with resistance to immune-mediated damage are 1) selection of cytokine-resistant cell lines by growth of INS-1 insulinoma cells in iteratively increasing concentrations of interleukin (IL)-1beta + gamma-interferon (IFN-gamma), and 2) stable overexpression of the anti-apoptotic gene bcl-2 in INS-1 cells. |
| 336 | 12765953 | Herein, we show that bcl-2-overexpressing cells are resistant to the cytotoxic effects of reactive oxygen and nitrogen species (ROS/RNS), but are only modestly protected against high concentrations of IL-1beta + INF-gamma, whereas the converse is true in cytokine selected cells. |
| 337 | 12765953 | We also found that the combination of bcl-2 expression and cytokine selection confers a broader spectrum of resistance than either procedure alone, such that the resultant cells are highly resistant to cytokines and ROS/RNS, with no impairment in glucose-stimulated insulin secretion. |
| 338 | 12765953 | INS-1-derived cells with combined bcl-2 expression and cytokine selection are also more resistant to damage induced by coculture with mitogen-activated peripheral blood mononuclear cells. |
| 339 | 12960095 | The peptide hormone, glucagon-like peptide 1 (GLP-1), has been shown to increase glucose-dependent insulin secretion, enhance insulin gene transcription, expand islet cell mass, and inhibit beta-cell apoptosis in animal models of diabetes. |
| 340 | 12960095 | Human islets were cultured for 5 d in the presence, or absence, of GLP-1 (10 nm, added every 12 h) and studied for viability and expression of proapoptotic (caspase-3) and antiapoptotic factors (bcl-2) as well as glucose-dependent insulin production. |
| 341 | 12960095 | The antiapoptotic effect of GLP-1 was associated with the down-regulation of active caspase-3 (P < 0.001) and the up-regulation of bcl-2 (P < 0.01). |
| 342 | 12960095 | The effect of GLP-1 on the intracellular levels of bcl-2 and caspase-3 was observed at the mRNA and protein levels. |
| 343 | 12960095 | Intracellular insulin content was markedly enhanced in islets cultured with GLP-1 vs. control (P < 0.001, at d 5), and there was a parallel GLP-1-dependent potentiation of glucose-dependent insulin secretion (P < 0.01 at d 3; P < 0.05 at d 5). |
| 344 | 12960095 | The peptide hormone, glucagon-like peptide 1 (GLP-1), has been shown to increase glucose-dependent insulin secretion, enhance insulin gene transcription, expand islet cell mass, and inhibit beta-cell apoptosis in animal models of diabetes. |
| 345 | 12960095 | Human islets were cultured for 5 d in the presence, or absence, of GLP-1 (10 nm, added every 12 h) and studied for viability and expression of proapoptotic (caspase-3) and antiapoptotic factors (bcl-2) as well as glucose-dependent insulin production. |
| 346 | 12960095 | The antiapoptotic effect of GLP-1 was associated with the down-regulation of active caspase-3 (P < 0.001) and the up-regulation of bcl-2 (P < 0.01). |
| 347 | 12960095 | The effect of GLP-1 on the intracellular levels of bcl-2 and caspase-3 was observed at the mRNA and protein levels. |
| 348 | 12960095 | Intracellular insulin content was markedly enhanced in islets cultured with GLP-1 vs. control (P < 0.001, at d 5), and there was a parallel GLP-1-dependent potentiation of glucose-dependent insulin secretion (P < 0.01 at d 3; P < 0.05 at d 5). |
| 349 | 12960095 | The peptide hormone, glucagon-like peptide 1 (GLP-1), has been shown to increase glucose-dependent insulin secretion, enhance insulin gene transcription, expand islet cell mass, and inhibit beta-cell apoptosis in animal models of diabetes. |
| 350 | 12960095 | Human islets were cultured for 5 d in the presence, or absence, of GLP-1 (10 nm, added every 12 h) and studied for viability and expression of proapoptotic (caspase-3) and antiapoptotic factors (bcl-2) as well as glucose-dependent insulin production. |
| 351 | 12960095 | The antiapoptotic effect of GLP-1 was associated with the down-regulation of active caspase-3 (P < 0.001) and the up-regulation of bcl-2 (P < 0.01). |
| 352 | 12960095 | The effect of GLP-1 on the intracellular levels of bcl-2 and caspase-3 was observed at the mRNA and protein levels. |
| 353 | 12960095 | Intracellular insulin content was markedly enhanced in islets cultured with GLP-1 vs. control (P < 0.001, at d 5), and there was a parallel GLP-1-dependent potentiation of glucose-dependent insulin secretion (P < 0.01 at d 3; P < 0.05 at d 5). |
| 354 | 14561487 | The JNK binding domain of islet-brain 1 inhibits IL-1 induced JNK activity and apoptosis but not the transcription of key proapoptotic or protective genes in insulin-secreting cell lines. |
| 355 | 14561487 | The stress-activated protein kinase c-Jun NH2-terminal kinase (JNK) is a central signal for interleukin-1beta (IL-1beta)-induced apoptosis in insulin-producing beta-cells. |
| 356 | 14561487 | The cell-permeable peptide inhibitor of JNK (JNKI1), that introduces the JNK binding domain (JBD) of the scaffold protein islet-brain 1 (IB1) inside cells, effectively prevents beta-cell death caused by this cytokine. |
| 357 | 14561487 | To define the molecular targets of JNK involved in cytokine-induced beta-cell apoptosis we investigated whether JNKI1 or stable expression of JBD affected the expression of selected pro- and anti-apoptotic genes induced in rat (RIN-5AH-T2B) and mouse (betaTC3) insulinoma cells exposed to IL-1beta. |
| 358 | 14561487 | Inhibition of JNK significantly reduced phosphorylation of the specific JNK substrate c-Jun (p<0.05), IL-1beta-induced apoptosis (p<0.001), and IL-1beta-mediated c-fos gene expression. |
| 359 | 14561487 | However, neither JNKI1 nor JBD did influence IL-1beta-induced NO synthesis or iNOS expression or the transcription of the genes encoding mitochondrial manganese superoxide dismutase (MnSOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase rho (GSTrho), heat shock protein (HSP) 70, IL-1beta-converting enzyme (ICE), caspase-3, apoptosis-inducing factor (AIF), Bcl-2 or Bcl-xL. |
| 360 | 14592444 | Tumor necrosis factor-alpha (TNF-alpha) is a cytokine considered to play a key role in beta-cell destruction in insulin-dependent diabetes mellitus (IDDM). |
| 361 | 14592444 | Expression of TNF receptor I, inducible form of nitric oxide synthase (iNOS), interleukin-1 beta-converting enzyme (ICE), Bcl-2, and nuclear factor kappa B (NF-kappa B) was analyzed by reverse transcriptase-polymerase chain reaction to investigate the suppressor mechanism of FTS on TNF-alpha-induced apoptosis. |
| 362 | 14592444 | FTS treatment suppressed the expression of iNOS and Bcl-2 mRNA in TNF-alpha-treated cells. |
| 363 | 14592444 | The expression of NF-kappa B mRNA in TNF-alpha-treated cells was enhanced after FTS treatment, while that of ICE mRNA did not change in TNF-alpha-treated cells with or without FTS treatment. |
| 364 | 14592444 | These results suggest that the inhibition of MIN6 cell death by FTS on TNF-alpha-induced apoptosis is caused by a negative feedback mechanism involving the inhibition of iNOS induction. |
| 365 | 14592444 | Tumor necrosis factor-alpha (TNF-alpha) is a cytokine considered to play a key role in beta-cell destruction in insulin-dependent diabetes mellitus (IDDM). |
| 366 | 14592444 | Expression of TNF receptor I, inducible form of nitric oxide synthase (iNOS), interleukin-1 beta-converting enzyme (ICE), Bcl-2, and nuclear factor kappa B (NF-kappa B) was analyzed by reverse transcriptase-polymerase chain reaction to investigate the suppressor mechanism of FTS on TNF-alpha-induced apoptosis. |
| 367 | 14592444 | FTS treatment suppressed the expression of iNOS and Bcl-2 mRNA in TNF-alpha-treated cells. |
| 368 | 14592444 | The expression of NF-kappa B mRNA in TNF-alpha-treated cells was enhanced after FTS treatment, while that of ICE mRNA did not change in TNF-alpha-treated cells with or without FTS treatment. |
| 369 | 14592444 | These results suggest that the inhibition of MIN6 cell death by FTS on TNF-alpha-induced apoptosis is caused by a negative feedback mechanism involving the inhibition of iNOS induction. |
| 370 | 14617576 | Insulin-like growth factor (IGF)-I/IGF-binding protein-3 complex: therapeutic efficacy and mechanism of protection against type 1 diabetes. |
| 371 | 14617576 | Administration of IGF-I either alone or as an IGF-I/IGFBP-3 complex reduced the severity of insulitis and delayed the onset of T1D in nonobese diabetic mice, but IGF-I/IGFBP-3 was significantly more effective. |
| 372 | 14617576 | Protection from T1D elicited by IGF-I/IGFBP-3 was mediated by up-regulated CCL4 and down-regulated CCL3 gene expression in pancreatic draining lymph nodes, activation of the phosphatidylinositol 3-kinase and Akt/protein kinase B signaling pathway of beta-cells, reduced beta-cell apoptosis, and stimulation of beta-cell replication. |
| 373 | 14617576 | Reduced beta-cell apoptosis resulted from elevated Bcl-2 and Bcl-X(L) activity and diminished caspase-9 activity, indicating a novel role for a mitochondrial-dependent pathway of beta-cell death. |
| 374 | 14617576 | Thus, IGF-I/IGFBP-3 affords more efficient protection from insulitis, beta-cell destruction, and T1D than IGF-I, and this complex may represent an efficacious therapeutic treatment for the prevention of T1D. |
| 375 | 14633857 | Activation of vascular endothelial growth factor receptor-1 sustains angiogenesis and Bcl-2 expression via the phosphatidylinositol 3-kinase pathway in endothelial cells. |
| 376 | 14633857 | Vascular insufficiency and retinal ischemia precede many proliferative retinopathies and stimulate secretion of various vasoactive growth factors, including vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF). |
| 377 | 14633857 | It is unclear, however, how PlGF, which is elevated in proliferative diabetic retinopathy and is a VEGF homolog that binds only to VEGF receptor (VEGFR)-1, promotes pathological angiogenesis. |
| 378 | 14633857 | When primary microvascular endothelial cells were grown on collagen gels, PlGF-containing ligands upregulated Bcl-2 expression and stimulated the formation of capillary-like tube networks that were retained for up to 14 days in culture. |
| 379 | 14633857 | In contrast, VEGF-induced tube formations and Bcl-2 expression were significantly decreased at the end of this period. |
| 380 | 14633857 | Flow cytometry analysis of annexin-V/propidium iodide-stained cells revealed that PlGF and PlGF/VEGF heterodimer inhibited apoptosis in serum-deprived endothelial cells. |
| 381 | 14633857 | These two growth factors stimulated a survival signaling pathway phosphatidylinositol 3-kinase (PI3K), as identified by increased Akt phosphorylation and because blocking PI3K signalling by adenovirus-mediated overexpression of wild-type phosphatase and tensin homolog on chromosome 10 (PTEN) disrupted angiogenesis and decreased Bcl-2 expression by PlGF and PlGF/VEGF heterodimer, whereas a dominant-negative PTEN mutant enhanced endothelial sprout formation and Bcl-2 expression. |
| 382 | 14633857 | Activation of vascular endothelial growth factor receptor-1 sustains angiogenesis and Bcl-2 expression via the phosphatidylinositol 3-kinase pathway in endothelial cells. |
| 383 | 14633857 | Vascular insufficiency and retinal ischemia precede many proliferative retinopathies and stimulate secretion of various vasoactive growth factors, including vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF). |
| 384 | 14633857 | It is unclear, however, how PlGF, which is elevated in proliferative diabetic retinopathy and is a VEGF homolog that binds only to VEGF receptor (VEGFR)-1, promotes pathological angiogenesis. |
| 385 | 14633857 | When primary microvascular endothelial cells were grown on collagen gels, PlGF-containing ligands upregulated Bcl-2 expression and stimulated the formation of capillary-like tube networks that were retained for up to 14 days in culture. |
| 386 | 14633857 | In contrast, VEGF-induced tube formations and Bcl-2 expression were significantly decreased at the end of this period. |
| 387 | 14633857 | Flow cytometry analysis of annexin-V/propidium iodide-stained cells revealed that PlGF and PlGF/VEGF heterodimer inhibited apoptosis in serum-deprived endothelial cells. |
| 388 | 14633857 | These two growth factors stimulated a survival signaling pathway phosphatidylinositol 3-kinase (PI3K), as identified by increased Akt phosphorylation and because blocking PI3K signalling by adenovirus-mediated overexpression of wild-type phosphatase and tensin homolog on chromosome 10 (PTEN) disrupted angiogenesis and decreased Bcl-2 expression by PlGF and PlGF/VEGF heterodimer, whereas a dominant-negative PTEN mutant enhanced endothelial sprout formation and Bcl-2 expression. |
| 389 | 14633857 | Activation of vascular endothelial growth factor receptor-1 sustains angiogenesis and Bcl-2 expression via the phosphatidylinositol 3-kinase pathway in endothelial cells. |
| 390 | 14633857 | Vascular insufficiency and retinal ischemia precede many proliferative retinopathies and stimulate secretion of various vasoactive growth factors, including vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF). |
| 391 | 14633857 | It is unclear, however, how PlGF, which is elevated in proliferative diabetic retinopathy and is a VEGF homolog that binds only to VEGF receptor (VEGFR)-1, promotes pathological angiogenesis. |
| 392 | 14633857 | When primary microvascular endothelial cells were grown on collagen gels, PlGF-containing ligands upregulated Bcl-2 expression and stimulated the formation of capillary-like tube networks that were retained for up to 14 days in culture. |
| 393 | 14633857 | In contrast, VEGF-induced tube formations and Bcl-2 expression were significantly decreased at the end of this period. |
| 394 | 14633857 | Flow cytometry analysis of annexin-V/propidium iodide-stained cells revealed that PlGF and PlGF/VEGF heterodimer inhibited apoptosis in serum-deprived endothelial cells. |
| 395 | 14633857 | These two growth factors stimulated a survival signaling pathway phosphatidylinositol 3-kinase (PI3K), as identified by increased Akt phosphorylation and because blocking PI3K signalling by adenovirus-mediated overexpression of wild-type phosphatase and tensin homolog on chromosome 10 (PTEN) disrupted angiogenesis and decreased Bcl-2 expression by PlGF and PlGF/VEGF heterodimer, whereas a dominant-negative PTEN mutant enhanced endothelial sprout formation and Bcl-2 expression. |
| 396 | 14633857 | Activation of vascular endothelial growth factor receptor-1 sustains angiogenesis and Bcl-2 expression via the phosphatidylinositol 3-kinase pathway in endothelial cells. |
| 397 | 14633857 | Vascular insufficiency and retinal ischemia precede many proliferative retinopathies and stimulate secretion of various vasoactive growth factors, including vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF). |
| 398 | 14633857 | It is unclear, however, how PlGF, which is elevated in proliferative diabetic retinopathy and is a VEGF homolog that binds only to VEGF receptor (VEGFR)-1, promotes pathological angiogenesis. |
| 399 | 14633857 | When primary microvascular endothelial cells were grown on collagen gels, PlGF-containing ligands upregulated Bcl-2 expression and stimulated the formation of capillary-like tube networks that were retained for up to 14 days in culture. |
| 400 | 14633857 | In contrast, VEGF-induced tube formations and Bcl-2 expression were significantly decreased at the end of this period. |
| 401 | 14633857 | Flow cytometry analysis of annexin-V/propidium iodide-stained cells revealed that PlGF and PlGF/VEGF heterodimer inhibited apoptosis in serum-deprived endothelial cells. |
| 402 | 14633857 | These two growth factors stimulated a survival signaling pathway phosphatidylinositol 3-kinase (PI3K), as identified by increased Akt phosphorylation and because blocking PI3K signalling by adenovirus-mediated overexpression of wild-type phosphatase and tensin homolog on chromosome 10 (PTEN) disrupted angiogenesis and decreased Bcl-2 expression by PlGF and PlGF/VEGF heterodimer, whereas a dominant-negative PTEN mutant enhanced endothelial sprout formation and Bcl-2 expression. |
| 403 | 14664702 | Diminished penile expression of vascular endothelial growth factor and its receptors at the insulin-resistant stage of a type II diabetic rat model: a possible cause for erectile dysfunction in diabetes. |
| 404 | 14664702 | We hypothesized that expressions of VEGF, its receptors and its signaling pathway Akt may be drastically altered in diabetic penile tIssues and their alterations may modulate penile expression of the molecules that are believed to play a role in diabetic ED. |
| 405 | 14664702 | We determined protein and mRNA expressions of VEGF, its receptors, Akt, nitric oxide synthase isoforms, and apoptosis-related molecules in the penis using immunohistochemistry, Western blotting, in situ hybridization, and real-time quantitative PCR analyses. |
| 406 | 14664702 | OLETF rats showed marked reductions in penile expression of VEGF, its two receptors and Akt. |
| 407 | 14664702 | Furthermore, while anti-apoptotic markers, Bcl-2 and phosphorylated Bad, were down-regulated, pro-apoptotic markers, active caspase-3 and Bax, were up-regulated, resulting in the appearance of apoptotic cells in the penile tIssues of OLETF rats. |
| 408 | 14690455 | Over-expression of sterol-regulatory-element-binding protein-1c (SREBP1c) in rat pancreatic islets induces lipogenesis and decreases glucose-stimulated insulin release: modulation by 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR). |
| 409 | 14690455 | In the present study, we determine whether over-expression in rat islets of the lipogenic transcription factor SREBP1c (sterol-regulatory-element-binding protein-1c) affects insulin release, and whether changes in islet lipid content may be reversed by activation of AMPK (AMP-activated protein kinase). |
| 410 | 14690455 | Real-time PCR (TaqMan) analysis showed that SREBP1c up-regulated the expression of FAS (fatty acid synthase; 6-fold), acetyl-CoA carboxylase-1 (2-fold), as well as peroxisomal-proliferator-activated receptor-gamma (7-fold), uncoupling protein-2 (1.4-fold) and Bcl2 (B-cell lymphocytic-leukaemia proto-oncogene 2; 1.3-fold). |
| 411 | 14690455 | By contrast, levels of pre-proinsulin, pancreatic duodenal homeobox-1, glucokinase and GLUT2 (glucose transporter isoform-2) mRNAs were unaltered. |
| 412 | 14690455 | Culture of islets with the AMPK activator 5-amino-4-imidazolecarboxamide riboside decreased the expression of the endogenous SREBP1c and FAS genes, and reversed the effect of over-expressing active SREBP1c on FAS mRNA levels and cellular triacylglycerol content. |
| 413 | 14702112 | mice; estrogen reduced tissue injury and enhanced antiapoptotic gene expression (bcl-2 and bfl-1). db/db mice demonstrated more damage, without increased bcl-2 mRNA; bfl-1 expression appeared at 48 hours of recovery associated with infarction. |
| 414 | 14702112 | Furthermore, estrogen replacement stimulated early postischemic expression of bcl-2 and bfl-1 and reduced damage in normoglycemic animals but failed to protect the diabetic brain. |
| 415 | 14702112 | mice; estrogen reduced tissue injury and enhanced antiapoptotic gene expression (bcl-2 and bfl-1). db/db mice demonstrated more damage, without increased bcl-2 mRNA; bfl-1 expression appeared at 48 hours of recovery associated with infarction. |
| 416 | 14702112 | Furthermore, estrogen replacement stimulated early postischemic expression of bcl-2 and bfl-1 and reduced damage in normoglycemic animals but failed to protect the diabetic brain. |
| 417 | 15114276 | LCPUFAs suppress the production of tumor necrosis factor-alpha (TNF-alpha) (and so also of OX40, since it belongs to the family of TNFR) and the expression of Bcl-2, suggesting that these fatty acids have the ability to prevent/suppress autoimmune diseases. |
| 418 | 15114276 | This indicates that LCPUFAs present in human breast milk suppress the levels of OX40 and decrease the expression of Bcl-xL and Bcl-2 on exposure to self-antigens and thus, protects against the development of autoimmune diseases in later life. |
| 419 | 15114276 | LCPUFAs suppress the production of tumor necrosis factor-alpha (TNF-alpha) (and so also of OX40, since it belongs to the family of TNFR) and the expression of Bcl-2, suggesting that these fatty acids have the ability to prevent/suppress autoimmune diseases. |
| 420 | 15114276 | This indicates that LCPUFAs present in human breast milk suppress the levels of OX40 and decrease the expression of Bcl-xL and Bcl-2 on exposure to self-antigens and thus, protects against the development of autoimmune diseases in later life. |
| 421 | 15298963 | Furthermore, diosgenin induced apoptosis in HT-29 cells at least in part by inhibition of bcl-2 and by induction of caspase-3 protein expression. |
| 422 | 15322087 | Guggulsterone inhibits NF-kappaB and IkappaBalpha kinase activation, suppresses expression of anti-apoptotic gene products, and enhances apoptosis. |
| 423 | 15322087 | Guggulsterone suppressed DNA binding of NF-kappaB induced by tumor necrosis factor (TNF), phorbol ester, okadaic acid, cigarette smoke condensate, hydrogen peroxide, and interleukin-1. |
| 424 | 15322087 | NF-kappaB-dependent reporter gene transcription induced by TNF, TNFR1, TRADD, TRAF2, NIK, and IKK was also blocked by guggulsterone but without affecting p65-mediated gene transcription. |
| 425 | 15322087 | In addition, guggulsterone decreased the expression of gene products involved in anti-apoptosis (IAP1, xIAP, Bfl-1/A1, Bcl-2, cFLIP, and survivin), proliferation (cyclin D1 and c-Myc), and metastasis (MMP-9, COX-2, and VEGF); this correlated with enhancement of apoptosis induced by TNF and chemotherapeutic agents. |
| 426 | 15369775 | It has been reported that overexpression of Bcl-2/Bcl-XL proteins enhances islet viability. |
| 427 | 15369775 | Bcl-XL and BH4 molecules were fused to TAT/PTD, the 11-aa cell penetrating peptide from HIV-1 transactivating protein, generating TAT-Bcl-XL and TAT-BH4, respectively. |
| 428 | 15369775 | Spontaneous caspase activation in human islets and cytotoxicity caused by IL-1beta were significantly reduced in the presence of TAT-Bcl-XL and TAT-BH4. |
| 429 | 15494484 | At 5-8 wk of age, even in the absence of TCRbeta expression, CD4+ and CD4+CD8+ blasts appear spontaneously. |
| 430 | 15494484 | They mimic normal beta selection by up-regulating germline TCR-Calpha transcripts, CD2, and Bcl-xL and down-regulating Bcl-2. |
| 431 | 15494484 | However, they fail to down-regulate transcription factors HEB-alt and Hes1 and initially express aberrantly high levels of Spi-B, c-kit (CD117), and IL-7Ralpha. |
| 432 | 15525583 | Rat islets treated with a cytokine combination (interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma) displayed a significant increase in islet cell apoptosis when the islets were incubated in 24.4 mM glucose compared with untreated islets at the same glucose concentration (13.07 +/- 1.78% vs 6.09 +/- 0.78%; P < 0.01) or islets incubated in 5.5 mM glucose concentration and cytokines (13.07 +/- 1.78% vs 8.04 +/- 1.56%; P < 0.05). |
| 433 | 15525583 | However, the expression of anti-apoptotic mediators such as bcl-2 and bcl-xL did not show any significant change. |
| 434 | 15525583 | These results suggest that cytokine- and STZ-mediated apoptotic effects on islet cells might be mediated by a glucose-induced hyperfunctional status and associated with an increase in Fas (Apo-1, CD-95) expression and no changes in the expression of the anti-apoptotic proteins bcl-xL and bcl-2. |
| 435 | 15525583 | Rat islets treated with a cytokine combination (interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma) displayed a significant increase in islet cell apoptosis when the islets were incubated in 24.4 mM glucose compared with untreated islets at the same glucose concentration (13.07 +/- 1.78% vs 6.09 +/- 0.78%; P < 0.01) or islets incubated in 5.5 mM glucose concentration and cytokines (13.07 +/- 1.78% vs 8.04 +/- 1.56%; P < 0.05). |
| 436 | 15525583 | However, the expression of anti-apoptotic mediators such as bcl-2 and bcl-xL did not show any significant change. |
| 437 | 15525583 | These results suggest that cytokine- and STZ-mediated apoptotic effects on islet cells might be mediated by a glucose-induced hyperfunctional status and associated with an increase in Fas (Apo-1, CD-95) expression and no changes in the expression of the anti-apoptotic proteins bcl-xL and bcl-2. |
| 438 | 15531378 | Since ischemia can be related to not only necrosis but apoptosis as well, we compared the development of apoptosis in STZ-diabetic rats and STZ-diabetic rats subjected to occlusion of the middle cerebral artery (MCA). 24-48 hr following MCA occlusion the animals were killed, the brain removed and prepared for evaluation by several indexes of apoptosis: nucleosomal DNA fragmentation, TUNEL staining, activation of caspase-3 and alteration in the expression of Bax and Bcl2. |
| 439 | 15565861 | Cells were transduced using a Maloney murine leukemia virus (MLV) vector coding for yellow fluorescent protein (YFP) and for one of the following antiapoptotic genes: cFLIP, FADD-DN, BcL-2, PI-9, and ICAM-2. |
| 440 | 15565861 | The data demonstrate that cFLIP, FADD-DN, and PI-9 are significantly more effective in protecting NIT-1 cells than BcL-2 and ICAM-2. |
| 441 | 15565861 | Additionally, the data show that despite its weak in vitro inhibition of caspase-3, PI-9 affords significant protection against TNF-alpha-induced apoptosis in these cells. |
| 442 | 15565861 | Cells were transduced using a Maloney murine leukemia virus (MLV) vector coding for yellow fluorescent protein (YFP) and for one of the following antiapoptotic genes: cFLIP, FADD-DN, BcL-2, PI-9, and ICAM-2. |
| 443 | 15565861 | The data demonstrate that cFLIP, FADD-DN, and PI-9 are significantly more effective in protecting NIT-1 cells than BcL-2 and ICAM-2. |
| 444 | 15565861 | Additionally, the data show that despite its weak in vitro inhibition of caspase-3, PI-9 affords significant protection against TNF-alpha-induced apoptosis in these cells. |
| 445 | 15582161 | Expression of the axotomy-responsive genes coding for growth-associated protein 43 (GAP-43), galanin, neuropeptide Y (NPY), pre-pro-vasoactive intestinal polypeptide (pre-pro-VIP), neuronal nitric oxide synthase (nNOS), protease nexin 1, heat-shock protein 27 (HSP 27) and myosin light chain kinase II (MLCK II) was unaffected in ganglia from diabetic rats compared to controls; thus, no axotomised phenotype was established. |
| 446 | 15582161 | The expression of the majority of proapoptotic genes in the DRG was also unaltered (bax, bad, bid, bok, c-Jun, p38, TNFR1, caspase 3 and NOS2). |
| 447 | 15582161 | Similarly there was no change in expression of the majority of antiapoptotic genes (bcl2, bcl-xL, bcl-w, NfkappaB). |
| 448 | 15587404 | This study examined the potential roles of astragalus and angiotensin II type 2 receptor (AT2) in rats with streptozotocin (STZ)-induced diabetic cardiomyopathy. |
| 449 | 15587404 | Cardiomyocyte apoptosis index (CAI), mRNA of AT2 and Bcl-2 as well as AT2 and Bcl-2 protein values in cardiomyocytes were also measured. |
| 450 | 15587404 | Changes of Bcl-2 were opposite to those of AT2. |
| 451 | 15587404 | This study examined the potential roles of astragalus and angiotensin II type 2 receptor (AT2) in rats with streptozotocin (STZ)-induced diabetic cardiomyopathy. |
| 452 | 15587404 | Cardiomyocyte apoptosis index (CAI), mRNA of AT2 and Bcl-2 as well as AT2 and Bcl-2 protein values in cardiomyocytes were also measured. |
| 453 | 15587404 | Changes of Bcl-2 were opposite to those of AT2. |
| 454 | 15595688 | [Apoptosis and the expression of Bax and Bcl-2 in the penis of diabetic rats]. |
| 455 | 15649569 | Immunohistochemical studies revealed that, in mirror sections, the staining of Bax and activated caspase-3 were observed in the TUNEL-positive cell area, but the expression of Bcl-2 in these apoptotic cells was generally too low to be detected. |
| 456 | 15649569 | These results suggest that a Bax-regulated mitochondrial cytochrome c-mediated caspase-3 activation pathway might be involved in the diabetic embryopathy. |
| 457 | 15677500 | Adenovirus-mediated XIAP gene transfer reverses the negative effects of immunosuppressive drugs on insulin secretion and cell viability of isolated human islets. |
| 458 | 15677500 | All three agents induce a decrease of intracellular levels of Bcl-2 and Bcl-xL, with an increased level of Smac, indicating that they are capable of promoting a downregulation of anti-apoptotic factors and an accumulation of pro-apoptotic mediators. |
| 459 | 15677500 | In conclusion, the present study demonstrates that genetically modified human islets expressing XIAP are resistant to the negative effects of immunosuppressive drugs on insulin secretion and cell viability. |
| 460 | 15677513 | High glucose inhibits apoptosis induced by serum deprivation in vascular smooth muscle cells via upregulation of Bcl-2 and Bcl-xl. |
| 461 | 15677513 | Furthermore, exposure of VSMCs to high glucose markedly increased the abundance of Bcl-2 and Bcl-xl mRNAs compared with treatment with normal glucose, while expression of bax and IAP-1 mRNA remained unchanged. |
| 462 | 15677513 | Our results suggest that high glucose suppresses serum withdrawal-induced apoptosis in VSMCs by upregulating expression of Bcl-2 and Bcl-xl, suggesting that enhanced expression of antiapoptotic proteins may play an important role in the development of macrovascular complications in diabetes. |
| 463 | 15677513 | High glucose inhibits apoptosis induced by serum deprivation in vascular smooth muscle cells via upregulation of Bcl-2 and Bcl-xl. |
| 464 | 15677513 | Furthermore, exposure of VSMCs to high glucose markedly increased the abundance of Bcl-2 and Bcl-xl mRNAs compared with treatment with normal glucose, while expression of bax and IAP-1 mRNA remained unchanged. |
| 465 | 15677513 | Our results suggest that high glucose suppresses serum withdrawal-induced apoptosis in VSMCs by upregulating expression of Bcl-2 and Bcl-xl, suggesting that enhanced expression of antiapoptotic proteins may play an important role in the development of macrovascular complications in diabetes. |
| 466 | 15677513 | High glucose inhibits apoptosis induced by serum deprivation in vascular smooth muscle cells via upregulation of Bcl-2 and Bcl-xl. |
| 467 | 15677513 | Furthermore, exposure of VSMCs to high glucose markedly increased the abundance of Bcl-2 and Bcl-xl mRNAs compared with treatment with normal glucose, while expression of bax and IAP-1 mRNA remained unchanged. |
| 468 | 15677513 | Our results suggest that high glucose suppresses serum withdrawal-induced apoptosis in VSMCs by upregulating expression of Bcl-2 and Bcl-xl, suggesting that enhanced expression of antiapoptotic proteins may play an important role in the development of macrovascular complications in diabetes. |
| 469 | 15705778 | We therefore generated a stable transfected beta-cell line (INS-1) overexpressing human TXNIP and found that TXNIP overexpression induced apoptosis as assessed by Bax, Bcl2, caspase-3, and cleaved caspase-9 as well as Hoechst staining. |
| 470 | 15705778 | Interestingly, islets of insulin-resistant/diabetic mice (AZIP-F1, BTBRob/ob) demonstrated elevated TXNIP expression, suggesting that TXNIP may play a role in glucotoxicity and the beta-cell loss observed under these conditions. |
| 471 | 15705778 | Thus, TXNIP is a novel proapoptotic beta-cell gene elevated in insulin resistance/diabetes and up-regulated by glucose through a unique ChoRE and may link glucotoxicity and beta-cell apoptosis. |
| 472 | 15784465 | Synergistic inhibition of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in human pancreatic beta cells by Bcl-2 and X-linked inhibitor of apoptosis. |
| 473 | 15784465 | To better understand the cytokine death-signal transduction pathways in human beta cells, we investigated the inhibitory effects of Bcl-2 (protooncogene bcl-2) and X-linked inhibitor of apoptosis (XIAP) on TRAIL (TNF-related apoptosis-inducing ligand)-induced human beta-cell destruction. |
| 474 | 15784465 | TRAIL-induced cytotoxicity and apoptosis of Bcl-2-overexpressing beta cells were clearly decreased, in comparison with wild-type cells and the empty vector transfectants. |
| 475 | 15784465 | Interestingly, cytotoxicity induced by TRAIL in human beta cells transfected with both Bcl-2 and AdXIAP was much less than that observed in human beta cells transfected with either Bcl-2 or XIAP alone (p < 0.005 in CM and p < 0.03 in NES2Y). |
| 476 | 15784465 | Overexpression of both Bcl-2 and XIAP inhibited TRAIL-induced activation of caspases as well as TRAIL-mediated damage of mitochondrial function in cells, suggesting possible regulatory mechanisms. |
| 477 | 15784465 | These results indicate that Bcl-2 and XIAP synergistically inhibit TRAIL-mediated death pathways in human beta cells. |
| 478 | 15784465 | Synergistic inhibition of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in human pancreatic beta cells by Bcl-2 and X-linked inhibitor of apoptosis. |
| 479 | 15784465 | To better understand the cytokine death-signal transduction pathways in human beta cells, we investigated the inhibitory effects of Bcl-2 (protooncogene bcl-2) and X-linked inhibitor of apoptosis (XIAP) on TRAIL (TNF-related apoptosis-inducing ligand)-induced human beta-cell destruction. |
| 480 | 15784465 | TRAIL-induced cytotoxicity and apoptosis of Bcl-2-overexpressing beta cells were clearly decreased, in comparison with wild-type cells and the empty vector transfectants. |
| 481 | 15784465 | Interestingly, cytotoxicity induced by TRAIL in human beta cells transfected with both Bcl-2 and AdXIAP was much less than that observed in human beta cells transfected with either Bcl-2 or XIAP alone (p < 0.005 in CM and p < 0.03 in NES2Y). |
| 482 | 15784465 | Overexpression of both Bcl-2 and XIAP inhibited TRAIL-induced activation of caspases as well as TRAIL-mediated damage of mitochondrial function in cells, suggesting possible regulatory mechanisms. |
| 483 | 15784465 | These results indicate that Bcl-2 and XIAP synergistically inhibit TRAIL-mediated death pathways in human beta cells. |
| 484 | 15784465 | Synergistic inhibition of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in human pancreatic beta cells by Bcl-2 and X-linked inhibitor of apoptosis. |
| 485 | 15784465 | To better understand the cytokine death-signal transduction pathways in human beta cells, we investigated the inhibitory effects of Bcl-2 (protooncogene bcl-2) and X-linked inhibitor of apoptosis (XIAP) on TRAIL (TNF-related apoptosis-inducing ligand)-induced human beta-cell destruction. |
| 486 | 15784465 | TRAIL-induced cytotoxicity and apoptosis of Bcl-2-overexpressing beta cells were clearly decreased, in comparison with wild-type cells and the empty vector transfectants. |
| 487 | 15784465 | Interestingly, cytotoxicity induced by TRAIL in human beta cells transfected with both Bcl-2 and AdXIAP was much less than that observed in human beta cells transfected with either Bcl-2 or XIAP alone (p < 0.005 in CM and p < 0.03 in NES2Y). |
| 488 | 15784465 | Overexpression of both Bcl-2 and XIAP inhibited TRAIL-induced activation of caspases as well as TRAIL-mediated damage of mitochondrial function in cells, suggesting possible regulatory mechanisms. |
| 489 | 15784465 | These results indicate that Bcl-2 and XIAP synergistically inhibit TRAIL-mediated death pathways in human beta cells. |
| 490 | 15784465 | Synergistic inhibition of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in human pancreatic beta cells by Bcl-2 and X-linked inhibitor of apoptosis. |
| 491 | 15784465 | To better understand the cytokine death-signal transduction pathways in human beta cells, we investigated the inhibitory effects of Bcl-2 (protooncogene bcl-2) and X-linked inhibitor of apoptosis (XIAP) on TRAIL (TNF-related apoptosis-inducing ligand)-induced human beta-cell destruction. |
| 492 | 15784465 | TRAIL-induced cytotoxicity and apoptosis of Bcl-2-overexpressing beta cells were clearly decreased, in comparison with wild-type cells and the empty vector transfectants. |
| 493 | 15784465 | Interestingly, cytotoxicity induced by TRAIL in human beta cells transfected with both Bcl-2 and AdXIAP was much less than that observed in human beta cells transfected with either Bcl-2 or XIAP alone (p < 0.005 in CM and p < 0.03 in NES2Y). |
| 494 | 15784465 | Overexpression of both Bcl-2 and XIAP inhibited TRAIL-induced activation of caspases as well as TRAIL-mediated damage of mitochondrial function in cells, suggesting possible regulatory mechanisms. |
| 495 | 15784465 | These results indicate that Bcl-2 and XIAP synergistically inhibit TRAIL-mediated death pathways in human beta cells. |
| 496 | 15784465 | Synergistic inhibition of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in human pancreatic beta cells by Bcl-2 and X-linked inhibitor of apoptosis. |
| 497 | 15784465 | To better understand the cytokine death-signal transduction pathways in human beta cells, we investigated the inhibitory effects of Bcl-2 (protooncogene bcl-2) and X-linked inhibitor of apoptosis (XIAP) on TRAIL (TNF-related apoptosis-inducing ligand)-induced human beta-cell destruction. |
| 498 | 15784465 | TRAIL-induced cytotoxicity and apoptosis of Bcl-2-overexpressing beta cells were clearly decreased, in comparison with wild-type cells and the empty vector transfectants. |
| 499 | 15784465 | Interestingly, cytotoxicity induced by TRAIL in human beta cells transfected with both Bcl-2 and AdXIAP was much less than that observed in human beta cells transfected with either Bcl-2 or XIAP alone (p < 0.005 in CM and p < 0.03 in NES2Y). |
| 500 | 15784465 | Overexpression of both Bcl-2 and XIAP inhibited TRAIL-induced activation of caspases as well as TRAIL-mediated damage of mitochondrial function in cells, suggesting possible regulatory mechanisms. |
| 501 | 15784465 | These results indicate that Bcl-2 and XIAP synergistically inhibit TRAIL-mediated death pathways in human beta cells. |
| 502 | 15784465 | Synergistic inhibition of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in human pancreatic beta cells by Bcl-2 and X-linked inhibitor of apoptosis. |
| 503 | 15784465 | To better understand the cytokine death-signal transduction pathways in human beta cells, we investigated the inhibitory effects of Bcl-2 (protooncogene bcl-2) and X-linked inhibitor of apoptosis (XIAP) on TRAIL (TNF-related apoptosis-inducing ligand)-induced human beta-cell destruction. |
| 504 | 15784465 | TRAIL-induced cytotoxicity and apoptosis of Bcl-2-overexpressing beta cells were clearly decreased, in comparison with wild-type cells and the empty vector transfectants. |
| 505 | 15784465 | Interestingly, cytotoxicity induced by TRAIL in human beta cells transfected with both Bcl-2 and AdXIAP was much less than that observed in human beta cells transfected with either Bcl-2 or XIAP alone (p < 0.005 in CM and p < 0.03 in NES2Y). |
| 506 | 15784465 | Overexpression of both Bcl-2 and XIAP inhibited TRAIL-induced activation of caspases as well as TRAIL-mediated damage of mitochondrial function in cells, suggesting possible regulatory mechanisms. |
| 507 | 15784465 | These results indicate that Bcl-2 and XIAP synergistically inhibit TRAIL-mediated death pathways in human beta cells. |
| 508 | 15800711 | The aim of our study was to determine whether synthetic ligands of PPARalpha and PPARgamma could affect the viability, proliferation, differentiation, apoptosis and expression of some cell cycle related proteins in glial tumor cell lines. |
| 509 | 15800711 | Cell lines were treated by ligands of PPARalpha (bezafibrate, gemfibrozil) and PPARgamma (ciglitazone). |
| 510 | 15800711 | The synthetic ligands significantly reduced or induced the expression of cyclins, p27Kip1, p21Waf1/Cip1, MDM-2, Bcl-2, Bax, PARP, Caspase 3, androgen receptors, etc. and did not affect the expression of the differentiation marker GFAP. |
| 511 | 15935144 | Emerging evidence implicates protein phosphatase 2A (PP2A) in the phenomenon of insulin secretion. |
| 512 | 15935144 | The three principal objectives of this commentary are to: (i) review the existing evidence, which suggests regulation, by glucose and other insulin secretagogues, of PP2A in the beta cell; (ii) discuss the experimental evidence, which implicates PP2A-like enzymes in the dephosphorylation and inactivation of key beta cell phosphoprotein substrates (e.g., Akt and Bcl-2), which may be necessary for beta cell proliferation and survival, culminating in the loss of the beta cell mass; and (iii) highlight potential avenues for future research, including the development of specific pharmacological and therapeutic interventional modalities for the inhibition of specific PP2A-like phosphatases for the prevention of loss of beta cell mass leading to the onset of diabetes. |
| 513 | 16021636 | T3 inhibited the apoptotic process induced by streptozocin, S-Nitroso-N-Acetylpenicylamine (SNAP), and H2O2 via regulation of the pro- and anti-apoptotic factors Bcl-2, Bcl-XL, Bad, Bax, and Caspase 3. |
| 514 | 16046294 | Mechanisms of compensatory beta-cell growth in insulin-resistant rats: roles of Akt kinase. |
| 515 | 16046294 | In these ZF pups, an augmented survival potential of beta-cells of ZF pups was observed by enhanced activated (phospho-) Akt, phospho-BAD, and Bcl-2 immunoreactivity in the postweaning period. |
| 516 | 16046294 | During this phase, we also detected an increase in the numbers of small beta-cell clusters among ducts and acini, increased duct pancreatic/duodenal homeobox-1 (PDX-1) immunoreactivity, and an increase in islet number in the ZF rats suggesting duct- and acini-mediated heightened beta-cell neogenesis. |
| 517 | 16046294 | Interestingly, in young ZF rats, specific cells associated with ducts, acini, and islets exhibited an increased frequency of PDX-1+/phospho-Akt+ staining, indicating a potential role for Akt in beta-cell differentiation. |
| 518 | 16111945 | Here we show that BEC-1, the C. elegans ortholog of the yeast and mammalian autophagy proteins Atg6/Vps30 and Beclin 1, is essential for development. |
| 519 | 16111945 | We demonstrate that BEC-1 is necessary for the function of the class III PI3 kinase LET-512/Vps34, an essential protein required for autophagy, membrane trafficking, and endocytosis. |
| 520 | 16111945 | Furthermore, BEC-1 forms a complex with the antiapoptotic protein CED-9/Bcl-2, and its depletion triggers CED-3/Caspase-dependent PCD. |
| 521 | 16114068 | Tumor necrosis factor-alpha-induced changes in insulin-producing beta-cells. |
| 522 | 16114068 | Similarly, in type 2 diabetes, the adipocyte-derived cytokines including TNF-alpha are elevated in the circulation, causing inflammation and insulin resistance. |
| 523 | 16114068 | We used RINr1046-38 (RIN) insulin-producing beta-cells, which constitutively express calbindin-D(28k), to characterize the effect of TNF-alpha on apoptosis, replication, insulin release, and gene and protein expression. |
| 524 | 16114068 | The subcellular localizations of Bcl-2, an antiapoptotic protein, and Bax, a proapoptotic protein, within RIN cells were altered with TNF-alpha treatment such that the two were colocalized with mitochondria in the perinuclear region. |
| 525 | 16227630 | From the list of 24 proteins differentially expressed between strains we identified two highly significant and interconnected networks centered around oncogenes (Myc and Mycn) and apoptosis-related genes (Bcl2 and Casp3). |
| 526 | 16227630 | They contained many of the same genes found in the proteome networks (including Myc and Mycn). |
| 527 | 16243419 | We investigated the apoptotic effects of polyphenols from red wine on human colon cancer cells SNU-C4 using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, 4,6-diamidino-2-phenylindole (DAPI) staining, terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay, reverse transcription-polymerase chain reaction (RT-PCR) expressions of Bcl-2, Bax and Caspase-3 genes, and Caspase-3 enzyme activity. |
| 528 | 16243419 | Compared with untreated control group, polyphenols (100 microg/ml) reduced the expression of Bcl-2 whereas those of Bax and Caspase-3 were increased. |
| 529 | 16243419 | We investigated the apoptotic effects of polyphenols from red wine on human colon cancer cells SNU-C4 using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, 4,6-diamidino-2-phenylindole (DAPI) staining, terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) assay, reverse transcription-polymerase chain reaction (RT-PCR) expressions of Bcl-2, Bax and Caspase-3 genes, and Caspase-3 enzyme activity. |
| 530 | 16243419 | Compared with untreated control group, polyphenols (100 microg/ml) reduced the expression of Bcl-2 whereas those of Bax and Caspase-3 were increased. |
| 531 | 16249459 | Nevertheless, nominally significant TDT results (P < 0.05) were obtained with polymorphisms in 20 genes, including 12 that have not been studied previously: aquaporin 1; B-cell leukemia/lymphoma 2 (bcl-2) proto-oncogene; catalase; glutathione peroxidase 1; IGF1; laminin alpha 4; laminin, gamma 1; SMAD, mothers against DPP homolog 3; transforming growth factor, beta receptor II; transforming growth factor, beta receptor III; tissue inhibitor of metalloproteinase 3; and upstream transcription factor 1. |
| 532 | 16254033 | Donor treatment with bilirubin up-regulated mRNA expression of protective genes such as HO-1 and bcl-2 and suppressed proinflammatory and proapoptotic genes including monocyte chemoattractant protein-1 and caspase-3 and -8 in the islet grafts before transplantation. |
| 533 | 16254033 | Furthermore, treatment of only the donor suppressed the expression of proinflammatory cytokines including TNF-alpha, inducible nitric oxide synthase, monocyte chemoattractant protein-1, and other proapoptotic and proinflammatory genes normally seen in the islets after transplantation. |
| 534 | 16265596 | This was associated by a decrease of the antiapoptotic protein Bcl-2, an increase of the pro-apoptotic protein Bax, and activation of caspase 3. |
| 535 | 16282055 | [Effects of liuwei dihuang pills on expressions of apoptosis-related genes bcl-2 and Bax in pancreas of OLETF rats]. |
| 536 | 16388709 | Plasma oxidant status, and expression of Bcl-2, activated NF-kB, inducible Nitric Oxide synthase (iNOS), and monocyte chemoattractant protein (MCP)-1 in circulating monocytes were evaluated at baseline and after 8-week oral vitamin E treatment (600 mg b.i.d.). |
| 537 | 16388709 | Bcl-2 down-regulation was associated with enhanced expression of NF-kB, iNOS and MCP-1, and showed a strong correlation with the albumin excretion rate. |
| 538 | 16388709 | Plasma oxidant status, and expression of Bcl-2, activated NF-kB, inducible Nitric Oxide synthase (iNOS), and monocyte chemoattractant protein (MCP)-1 in circulating monocytes were evaluated at baseline and after 8-week oral vitamin E treatment (600 mg b.i.d.). |
| 539 | 16388709 | Bcl-2 down-regulation was associated with enhanced expression of NF-kB, iNOS and MCP-1, and showed a strong correlation with the albumin excretion rate. |
| 540 | 16394503 | MCTF treatment activated caspase-8, -9 and -3, and led to cleaved poly (ADP-ribose) polymerase and release of cytochrome c into cytosol in a concentration-dependent manner, while MCTF did not affect Bax or Bcl-2 protein levels as shown by Western blot analysis. |
| 541 | 16394656 | Role of Bim and other Bcl-2 family members in autoimmune and degenerative diseases. |
| 542 | 16446153 | Bcl-2, Bid, and Bad inhibit assembly sub-stoichiometrically, whereas peptides from Bak and Bax promote tubulin polymerization at near stoichiometric concentrations. |
| 543 | 16644678 | Human IMA VSMCs from diabetic patients showed resistance to apoptosis, measured as DNA fragmentation and caspase-3 activation, induced by C-reactive protein (CRP) and other stimuli, such as hydrogen peroxide and 7beta-hydroxycholesterol. |
| 544 | 16644678 | Consistent with the above, we found that pretreatment of nondiabetic VSMCs with high glucose abolished the degradation of Bcl-2 induced by CRP. |
| 545 | 16644695 | In INS-1 cells, dexamethasone increased the number of transferase-mediated dUTP nick-end labeling-staining positive cells, caspase-3 activity, and poly-(ADP-) ribose polymerase protein cleavage; decreased Bcl-2 transcript and protein abundance; dephosphorylated the proapoptotic protein of the Bcl-2 family (BAD) at serine155; and depolarized mitochondria. |
| 546 | 16644695 | In conclusion, glucocorticoid-induced apoptosis in insulin-secreting cells is accompanied by a downregulation of Bcl-2, activation of calcineurin with subsequent dephosphorylation of BAD, and mitochondrial depolarization. |
| 547 | 16644695 | In INS-1 cells, dexamethasone increased the number of transferase-mediated dUTP nick-end labeling-staining positive cells, caspase-3 activity, and poly-(ADP-) ribose polymerase protein cleavage; decreased Bcl-2 transcript and protein abundance; dephosphorylated the proapoptotic protein of the Bcl-2 family (BAD) at serine155; and depolarized mitochondria. |
| 548 | 16644695 | In conclusion, glucocorticoid-induced apoptosis in insulin-secreting cells is accompanied by a downregulation of Bcl-2, activation of calcineurin with subsequent dephosphorylation of BAD, and mitochondrial depolarization. |
| 549 | 16647092 | The levels of Bax, a pro-apoptotic member of Bcl-2 family, appeared increased at baseline in mast cells from diabetic rats compared with normal cells. |
| 550 | 16674981 | The results showed that AGE-BSA could induce significantly the apoptosis of BRPs in a dose-dependent manner compared with controls, associated with an increase in intracellular malondialdehyde level and caspase-3 activity; a decrease in intracellular catalase, SOD activities and Bcl-2/Bax ratio. |
| 551 | 16674981 | The decreased Bcl-2/Bax ratio and activation of caspase-3 are associated with apoptotic process. |
| 552 | 16674981 | The results showed that AGE-BSA could induce significantly the apoptosis of BRPs in a dose-dependent manner compared with controls, associated with an increase in intracellular malondialdehyde level and caspase-3 activity; a decrease in intracellular catalase, SOD activities and Bcl-2/Bax ratio. |
| 553 | 16674981 | The decreased Bcl-2/Bax ratio and activation of caspase-3 are associated with apoptotic process. |
| 554 | 16731829 | Thiazolidinediones are ligands for peroxisome proliferator-activated receptor (PPAR)-gamma, widely used as insulin sensitizer in type 2 diabetic patients and implicated in apoptosis, cell proliferation, and cell cycle regulation. |
| 555 | 16731829 | Although similar HbA(1c) levels were observed in both groups, pioglitazone significantly inhibited glomerular hypertrophy and mesangial matrix expansion and reduced urinary albumin excretion compared with the insulin-treated group. |
| 556 | 16731829 | In addition, pioglitazone significantly reduced the number of glomerular p27(Kip1)-positive cells. |
| 557 | 16731829 | Pioglitazone suppressed high glucose-induced phosphorylation of p44/42 mitogen-activated protein kinase and reduced Bcl-2 and p27(Kip1) protein levels. |
| 558 | 16780994 | After small and large dosage (1 or 10mg/kg/d) carvedilol-administrated for 5 weeks, hemodynamic parameters, the levels of malondialdehyde (MDA), the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and expression of Bcl-2 mRNA in the cardiac tissues of all six groups were measured. |
| 559 | 16873684 | cAMP-responsive element-binding protein (CREB) is required for beta-cell survival by regulating expression of crucial genes such as bcl-2 and IRS-2. |
| 560 | 16873684 | We observed that 10 mmol/l glucose-induced CREB phosphorylation was totally inhibited by the protein kinase A (PKA) inhibitor H89 (2 micromol/l) and reduced by 50% with the extracellular signal-regulated kinase (ERK)1/2 inhibitor PD98059 (20 micromol/l). |
| 561 | 16873684 | This indicates that ERK1/2, reported to be located downstream of PKA, participates in the PKA-mediated CREB phosphorylation elicited by glucose. |
| 562 | 16873684 | In ERK1/2-downregulated MIN6 cells by siRNA, glucose-stimulated CREB phosphorylation was highly reduced and CREB protein content was decreased by 60%. |
| 563 | 16873684 | In MIN6 cells and islets cultured for 24-48 h in optimal glucose concentration (10 mmol/l), which promotes survival, blockade of ERK1/2 activity with PD98059 caused a significant decrease in CREB protein level, whereas CREB mRNA remained unaffected (measured by real-time quantitative PCR). |
| 564 | 16873684 | This was associated with loss of bcl-2 mRNA and protein contents, caspase-3 activation, and emergence of ultrastructural apoptotic features detected by electron microscopy. |
| 565 | 16873684 | Our results indicate that ERK1 and -2 control the phosphorylation and protein level of CREB and play a key role in glucose-mediated pancreatic beta-cell survival. |
| 566 | 16873684 | cAMP-responsive element-binding protein (CREB) is required for beta-cell survival by regulating expression of crucial genes such as bcl-2 and IRS-2. |
| 567 | 16873684 | We observed that 10 mmol/l glucose-induced CREB phosphorylation was totally inhibited by the protein kinase A (PKA) inhibitor H89 (2 micromol/l) and reduced by 50% with the extracellular signal-regulated kinase (ERK)1/2 inhibitor PD98059 (20 micromol/l). |
| 568 | 16873684 | This indicates that ERK1/2, reported to be located downstream of PKA, participates in the PKA-mediated CREB phosphorylation elicited by glucose. |
| 569 | 16873684 | In ERK1/2-downregulated MIN6 cells by siRNA, glucose-stimulated CREB phosphorylation was highly reduced and CREB protein content was decreased by 60%. |
| 570 | 16873684 | In MIN6 cells and islets cultured for 24-48 h in optimal glucose concentration (10 mmol/l), which promotes survival, blockade of ERK1/2 activity with PD98059 caused a significant decrease in CREB protein level, whereas CREB mRNA remained unaffected (measured by real-time quantitative PCR). |
| 571 | 16873684 | This was associated with loss of bcl-2 mRNA and protein contents, caspase-3 activation, and emergence of ultrastructural apoptotic features detected by electron microscopy. |
| 572 | 16873684 | Our results indicate that ERK1 and -2 control the phosphorylation and protein level of CREB and play a key role in glucose-mediated pancreatic beta-cell survival. |
| 573 | 16939413 | Cytochrome c release from the mitochondrial intermembrane space into the cytosol was increased significantly in lymphocytes from fasted rats cultured for 24 h, whereas the levels of bcl-2 and bax proteins were not affected. |
| 574 | 16951721 | American ginseng stimulates insulin production and prevents apoptosis through regulation of uncoupling protein-2 in cultured beta cells. |
| 575 | 16951721 | A mitochondrial protein, uncoupling protein-2 (UCP-2) has been found to play a critical role in insulin synthesis and beta cell survival. |
| 576 | 16951721 | Our preliminary studies found that the extracts of American ginseng inhibit UCP-2 expression which may contribute to the ability of ginseng protecting beta cell death and improving insulin synthesis. |
| 577 | 16951721 | Therefore, we hypothesized that ginseng extracts suppress UCP-2 in the mitochondria of pancreatic beta cells, promoting insulin synthesis and anti-apoptosis (a programmed cell-death mechanism). |
| 578 | 16951721 | We evaluated effects of ginseng on UCP-2 expression, insulin production, anti-/pro-apoptotic factors Bcl-2/caspase-9 expression and cellular ATP levels. |
| 579 | 16951721 | We found that ginseng suppresses UCP-2, down-regulates caspase-9 while increasing ATP and insulin production/secretion and up-regulates Bcl-2, reducing apoptosis. |
| 580 | 16951721 | These findings suggest that stimulation of insulin production and prevention of beta cell loss by American ginseng extracts can occur via the inhibition of mitochondrial UCP-2, resulting in increase in the ATP level and the anti-apoptotic factor Bcl-2, while down-regulation of pro-apoptotic factor caspase-9 occurs, lowering the occurrence of apoptosis, which support the hypothesis. |
| 581 | 16951721 | American ginseng stimulates insulin production and prevents apoptosis through regulation of uncoupling protein-2 in cultured beta cells. |
| 582 | 16951721 | A mitochondrial protein, uncoupling protein-2 (UCP-2) has been found to play a critical role in insulin synthesis and beta cell survival. |
| 583 | 16951721 | Our preliminary studies found that the extracts of American ginseng inhibit UCP-2 expression which may contribute to the ability of ginseng protecting beta cell death and improving insulin synthesis. |
| 584 | 16951721 | Therefore, we hypothesized that ginseng extracts suppress UCP-2 in the mitochondria of pancreatic beta cells, promoting insulin synthesis and anti-apoptosis (a programmed cell-death mechanism). |
| 585 | 16951721 | We evaluated effects of ginseng on UCP-2 expression, insulin production, anti-/pro-apoptotic factors Bcl-2/caspase-9 expression and cellular ATP levels. |
| 586 | 16951721 | We found that ginseng suppresses UCP-2, down-regulates caspase-9 while increasing ATP and insulin production/secretion and up-regulates Bcl-2, reducing apoptosis. |
| 587 | 16951721 | These findings suggest that stimulation of insulin production and prevention of beta cell loss by American ginseng extracts can occur via the inhibition of mitochondrial UCP-2, resulting in increase in the ATP level and the anti-apoptotic factor Bcl-2, while down-regulation of pro-apoptotic factor caspase-9 occurs, lowering the occurrence of apoptosis, which support the hypothesis. |
| 588 | 16951721 | American ginseng stimulates insulin production and prevents apoptosis through regulation of uncoupling protein-2 in cultured beta cells. |
| 589 | 16951721 | A mitochondrial protein, uncoupling protein-2 (UCP-2) has been found to play a critical role in insulin synthesis and beta cell survival. |
| 590 | 16951721 | Our preliminary studies found that the extracts of American ginseng inhibit UCP-2 expression which may contribute to the ability of ginseng protecting beta cell death and improving insulin synthesis. |
| 591 | 16951721 | Therefore, we hypothesized that ginseng extracts suppress UCP-2 in the mitochondria of pancreatic beta cells, promoting insulin synthesis and anti-apoptosis (a programmed cell-death mechanism). |
| 592 | 16951721 | We evaluated effects of ginseng on UCP-2 expression, insulin production, anti-/pro-apoptotic factors Bcl-2/caspase-9 expression and cellular ATP levels. |
| 593 | 16951721 | We found that ginseng suppresses UCP-2, down-regulates caspase-9 while increasing ATP and insulin production/secretion and up-regulates Bcl-2, reducing apoptosis. |
| 594 | 16951721 | These findings suggest that stimulation of insulin production and prevention of beta cell loss by American ginseng extracts can occur via the inhibition of mitochondrial UCP-2, resulting in increase in the ATP level and the anti-apoptotic factor Bcl-2, while down-regulation of pro-apoptotic factor caspase-9 occurs, lowering the occurrence of apoptosis, which support the hypothesis. |
| 595 | 16959961 | Increased HO activity was also associated with a significant increase in the antiapoptotic signaling molecules Bcl-xl and phosphorylation of p38-mitogen-activated protein kinase but no significant increases in Bcl-2 or BAD proteins. |
| 596 | 17034987 | We found decreased Bcl-2, increased Bax and cleaved Caspase 3 proteins in embryos from diabetic rats. |
| 597 | 17053028 | Diazoxide prevents diabetes through inhibiting pancreatic beta-cells from apoptosis via Bcl-2/Bax rate and p38-beta mitogen-activated protein kinase. |
| 598 | 17053028 | Further study demonstrated that diazoxide up-regulated Bcl-2 expression and p38beta MAPK, which expressed at very low levels due to the high glucose, but not c-jun N-terminal kinase and ERK. |
| 599 | 17053028 | In this study, we demonstrate that diazoxide prevents the onset and development of diabetes in OLETF rats by inhibiting beta-cell apoptosis via increasing p38beta MAPK, elevating Bcl-2/Bax ratio, and ameliorating insulin secretory capacity and action. |
| 600 | 17053028 | Diazoxide prevents diabetes through inhibiting pancreatic beta-cells from apoptosis via Bcl-2/Bax rate and p38-beta mitogen-activated protein kinase. |
| 601 | 17053028 | Further study demonstrated that diazoxide up-regulated Bcl-2 expression and p38beta MAPK, which expressed at very low levels due to the high glucose, but not c-jun N-terminal kinase and ERK. |
| 602 | 17053028 | In this study, we demonstrate that diazoxide prevents the onset and development of diabetes in OLETF rats by inhibiting beta-cell apoptosis via increasing p38beta MAPK, elevating Bcl-2/Bax ratio, and ameliorating insulin secretory capacity and action. |
| 603 | 17053028 | Diazoxide prevents diabetes through inhibiting pancreatic beta-cells from apoptosis via Bcl-2/Bax rate and p38-beta mitogen-activated protein kinase. |
| 604 | 17053028 | Further study demonstrated that diazoxide up-regulated Bcl-2 expression and p38beta MAPK, which expressed at very low levels due to the high glucose, but not c-jun N-terminal kinase and ERK. |
| 605 | 17053028 | In this study, we demonstrate that diazoxide prevents the onset and development of diabetes in OLETF rats by inhibiting beta-cell apoptosis via increasing p38beta MAPK, elevating Bcl-2/Bax ratio, and ameliorating insulin secretory capacity and action. |
| 606 | 17131386 | Apoptotic signaling in methylglyoxal-treated human osteoblasts involves oxidative stress, c-Jun N-terminal kinase, caspase-3, and p21-activated kinase 2. |
| 607 | 17131386 | We further show that MG-induced apoptosis of osteoblasts involves specific apoptotic biochemical changes, including oxidative stress, c-Jun N-terminal kinase (JNK) activation, mitochondrial membrane potential changes, cytochrome C release, increased Bax/Bcl-2 protein ratios, and activation of caspases (caspase-9, caspase-3) and p21-activated protein kinase 2 (PAK2). |
| 608 | 17131386 | Treatment of osteoblasts with SP600125, a JNK-specific inhibitor, led to a reduction in MG-induced apoptosis and decreased activation of caspase-3 and PAK2, indicating that JNK activity is upstream of these events. |
| 609 | 17131386 | Experiments using anti-sense oligonucleotides against PAK2 further showed that PAK2 activation is required for MG-induced apoptosis in osteoblasts. |
| 610 | 17210759 | Activation of caspase 3 decreased and anti-apoptotic members of the Bcl-2 protein family increased as early as 1 week after diabetes onset. |
| 611 | 17242177 | Simultaneous administration of HGF and FFAs significantly suppressed the impaired insulin secretion and FFA-induced apoptosis. |
| 612 | 17242177 | These effects appear to be mediated by bcl-2 and phosphatidylinositol 3 kinase (PI3K)/Akt pathways. |
| 613 | 17242177 | Indeed, HGF increased mRNA and protein expression of bcl-2 downregulated by FFAs-treatment; moreover, pre-treatment with the specific PI3-kinase inhibitor LY294002, significantly abolished the protective effect of HGF. |
| 614 | 17242177 | In conclusion, in rat insulin-producing RINm5F cells, HGF exerts its prosurvival effect by counteracting the increased intracellular oxidative stress and, consequently, by inhibiting apoptosis induced by chronic exposure to FFAs. |
| 615 | 17242177 | Simultaneous administration of HGF and FFAs significantly suppressed the impaired insulin secretion and FFA-induced apoptosis. |
| 616 | 17242177 | These effects appear to be mediated by bcl-2 and phosphatidylinositol 3 kinase (PI3K)/Akt pathways. |
| 617 | 17242177 | Indeed, HGF increased mRNA and protein expression of bcl-2 downregulated by FFAs-treatment; moreover, pre-treatment with the specific PI3-kinase inhibitor LY294002, significantly abolished the protective effect of HGF. |
| 618 | 17242177 | In conclusion, in rat insulin-producing RINm5F cells, HGF exerts its prosurvival effect by counteracting the increased intracellular oxidative stress and, consequently, by inhibiting apoptosis induced by chronic exposure to FFAs. |
| 619 | 17482424 | We aimed to investigate the extent to which maternal diabetes with or without folic acid (FA) supplementation affects mRNA levels and protein distribution of ROS scavenging enzymes, vascular endothelial growth factor-A (Vegf-A), folate binding protein-1 (Folbp-1), and apoptosis-associated proteins in the yolk sacs of rat embryos on gestational days 10 and 11. |
| 620 | 17482424 | Maternal diabetes also increased the levels of CuZnSOD protein, increased the Bax/Bcl-2 protein ratio and decreased Vegf-A protein distribution. |
| 621 | 17482424 | FA treatment normalized vascular morphology, decreased mRNA levels of all three SOD isoforms and increased Vegf-A mRNA levels, rectified CuZnSOD protein distribution and Bax/Bcl-2 ratio. |
| 622 | 17482424 | We aimed to investigate the extent to which maternal diabetes with or without folic acid (FA) supplementation affects mRNA levels and protein distribution of ROS scavenging enzymes, vascular endothelial growth factor-A (Vegf-A), folate binding protein-1 (Folbp-1), and apoptosis-associated proteins in the yolk sacs of rat embryos on gestational days 10 and 11. |
| 623 | 17482424 | Maternal diabetes also increased the levels of CuZnSOD protein, increased the Bax/Bcl-2 protein ratio and decreased Vegf-A protein distribution. |
| 624 | 17482424 | FA treatment normalized vascular morphology, decreased mRNA levels of all three SOD isoforms and increased Vegf-A mRNA levels, rectified CuZnSOD protein distribution and Bax/Bcl-2 ratio. |
| 625 | 17487332 | Central tolerance seems to rely more heavily on the mitochondria-based, T cell receptor (TCR)-stimulated apoptotic pathway, since thymocytes lacking the pro-apoptotic Bcl-2 family member Bim are resistant to TCR-induced apoptosis. |
| 626 | 17569614 | Resveratrol induces apoptosis by up-regulating the expression of Bax, Bak, PUMA, Noxa, Bim, p53, TRAIL, TRAIL-R1/DR4 and TRAIL-R2/DR5 and simultaneously down-regulating the expression of Bcl-2, Bcl-XL, Mcl-1 and survivin. |
| 627 | 17569614 | Resveratrol causes growth arrest at G1 and G1/S phases of cell cycle by inducing the expression of CDK inhibitors p21/WAF1/CIP1 and p27/KIP1. |
| 628 | 17612655 | Insulin deficient cells succumbed to apoptosis, an effect associated with impaired PI3-kinase/Akt signaling and reduction in the Bcl-2 to Bax ratio. |
| 629 | 17652910 | In Western blot analysis, the ratio of Bax/Bcl-2 protein expression in cells treated with high glucose was significantly increased compared to controls. |
| 630 | 17693608 | Co-chaperone potentiation of vitamin D receptor-mediated transactivation: a role for Bcl2-associated athanogene-1 as an intracellular-binding protein for 1,25-dihydroxyvitamin D3. |
| 631 | 17693608 | Hsc70 also recruits and interacts with the co-chaperone Bcl2-associated athanogene (BAG)-1 via the ATP-binding domain that resides on hsc70. |
| 632 | 17693608 | To investigate the functional significance of this, we transiently overexpressed the S, M, and L variants of BAG-1 into human kidney HKC-8 cells stably transfected with a 1,25(OH)2D3-responsive 24-hydroxylase (CYP24) promoter-reporter construct. |
| 633 | 17693608 | These data highlight a novel role for BAG-1 as an intracellular-binding protein for 1,25(OH)2D3 and further suggest that BAG-1 is able to potentiate vitamin D receptor-mediated transactivation by acting as a nuclear chaperone for 1,25(OH)2D3. |
| 634 | 17693608 | Co-chaperone potentiation of vitamin D receptor-mediated transactivation: a role for Bcl2-associated athanogene-1 as an intracellular-binding protein for 1,25-dihydroxyvitamin D3. |
| 635 | 17693608 | Hsc70 also recruits and interacts with the co-chaperone Bcl2-associated athanogene (BAG)-1 via the ATP-binding domain that resides on hsc70. |
| 636 | 17693608 | To investigate the functional significance of this, we transiently overexpressed the S, M, and L variants of BAG-1 into human kidney HKC-8 cells stably transfected with a 1,25(OH)2D3-responsive 24-hydroxylase (CYP24) promoter-reporter construct. |
| 637 | 17693608 | These data highlight a novel role for BAG-1 as an intracellular-binding protein for 1,25(OH)2D3 and further suggest that BAG-1 is able to potentiate vitamin D receptor-mediated transactivation by acting as a nuclear chaperone for 1,25(OH)2D3. |
| 638 | 17870134 | The levels of Bcl-2 and Bcl-X(L), anti-apoptotic proteins, were decreased in the diabetic group. |
| 639 | 17870134 | Our findings suggest that streptozotocin-induced diabetes increases apoptotic cell death in testis tissue through the up-and down-regulation of Bcl-2 family proteins and the interaction of Bad and Bcl-X(L). |
| 640 | 17870134 | The levels of Bcl-2 and Bcl-X(L), anti-apoptotic proteins, were decreased in the diabetic group. |
| 641 | 17870134 | Our findings suggest that streptozotocin-induced diabetes increases apoptotic cell death in testis tissue through the up-and down-regulation of Bcl-2 family proteins and the interaction of Bad and Bcl-X(L). |
| 642 | 17876565 | Apoptosis was evaluated by annexin V, by poly(ADP-ribose) polymerase protein cleavage, and cyclooxygenase-2 (COX-2), Bax/Bcl-2, and p53 protein levels; proliferation was assessed by determining cell cycle phase distribution and the amounts of the cell cycle regulators E2F1, cyclin D1, E1, and A and the levels of the hyper-phosphorylated form of the retinoblastoma protein (ppRb). |
| 643 | 17876565 | HG resulted in increased (p<0.05) apoptosis rate associated with COX-2 protein overexpression, without modification of Bax/Bcl2 ratio and p53 levels. |
| 644 | 17876565 | Both in HG and NG, fenofibrate dramatically reduced cell proliferation (p<0.05) through a G1/G0 block mediated by the reduction in ppRb and the decrease in E2F1, cyclin E1, A, and D1 protein expression, with a mechanism that, for cyclin E1, occurred at the posttranscriptional level. |
| 645 | 17876565 | Apoptosis was evaluated by annexin V, by poly(ADP-ribose) polymerase protein cleavage, and cyclooxygenase-2 (COX-2), Bax/Bcl-2, and p53 protein levels; proliferation was assessed by determining cell cycle phase distribution and the amounts of the cell cycle regulators E2F1, cyclin D1, E1, and A and the levels of the hyper-phosphorylated form of the retinoblastoma protein (ppRb). |
| 646 | 17876565 | HG resulted in increased (p<0.05) apoptosis rate associated with COX-2 protein overexpression, without modification of Bax/Bcl2 ratio and p53 levels. |
| 647 | 17876565 | Both in HG and NG, fenofibrate dramatically reduced cell proliferation (p<0.05) through a G1/G0 block mediated by the reduction in ppRb and the decrease in E2F1, cyclin E1, A, and D1 protein expression, with a mechanism that, for cyclin E1, occurred at the posttranscriptional level. |
| 648 | 17880809 | [Analysis of intracellular proapoptotic (Bax, Bak) and antiapoptotic (Bcl-2, Bcl-XL) proteins expression in thyrocytes from young patients with immune and non-immune thyroid disorders]. |
| 649 | 17880809 | The aim of this study was to estimate the expression of proapoptotic (Bax, Bak) and antiapoptotic (Bcl-2, Bcl-XL) proteins in thyroid tissues from 12 patients with Graves' disease (GD), 10 with non-toxic nodular goitre (NTNG) and 10 with toxic nodular goitre (TNG). |
| 650 | 17880809 | Identification of antiapoptotic Bcl-2 and Bcl-XL molecules in the thyroid follicular cells revealed a higher expression of both proteins in patients with Graves' disease (+++; ++, respectively) in comparison to patients with NTNG (++/+; +) and TNG (++; +). |
| 651 | 17880809 | The detection of proapoptotic molecules showed higher expression of Bak (++/+) and Bax (+) in Graves' thyroid tissues while Bax was in trace amount in NTNG (0/+) and TNG (0/+). |
| 652 | 17880809 | [Analysis of intracellular proapoptotic (Bax, Bak) and antiapoptotic (Bcl-2, Bcl-XL) proteins expression in thyrocytes from young patients with immune and non-immune thyroid disorders]. |
| 653 | 17880809 | The aim of this study was to estimate the expression of proapoptotic (Bax, Bak) and antiapoptotic (Bcl-2, Bcl-XL) proteins in thyroid tissues from 12 patients with Graves' disease (GD), 10 with non-toxic nodular goitre (NTNG) and 10 with toxic nodular goitre (TNG). |
| 654 | 17880809 | Identification of antiapoptotic Bcl-2 and Bcl-XL molecules in the thyroid follicular cells revealed a higher expression of both proteins in patients with Graves' disease (+++; ++, respectively) in comparison to patients with NTNG (++/+; +) and TNG (++; +). |
| 655 | 17880809 | The detection of proapoptotic molecules showed higher expression of Bak (++/+) and Bax (+) in Graves' thyroid tissues while Bax was in trace amount in NTNG (0/+) and TNG (0/+). |
| 656 | 17880809 | [Analysis of intracellular proapoptotic (Bax, Bak) and antiapoptotic (Bcl-2, Bcl-XL) proteins expression in thyrocytes from young patients with immune and non-immune thyroid disorders]. |
| 657 | 17880809 | The aim of this study was to estimate the expression of proapoptotic (Bax, Bak) and antiapoptotic (Bcl-2, Bcl-XL) proteins in thyroid tissues from 12 patients with Graves' disease (GD), 10 with non-toxic nodular goitre (NTNG) and 10 with toxic nodular goitre (TNG). |
| 658 | 17880809 | Identification of antiapoptotic Bcl-2 and Bcl-XL molecules in the thyroid follicular cells revealed a higher expression of both proteins in patients with Graves' disease (+++; ++, respectively) in comparison to patients with NTNG (++/+; +) and TNG (++; +). |
| 659 | 17880809 | The detection of proapoptotic molecules showed higher expression of Bak (++/+) and Bax (+) in Graves' thyroid tissues while Bax was in trace amount in NTNG (0/+) and TNG (0/+). |
| 660 | 17978676 | [Expression of Bax and Bcl-2 apoptotic factors in the conjunctiva of diabetic patients: a preliminary study]. |
| 661 | 17997942 | [Effects of resolving stagnation and promoting granulation therapy on expressions of Bax and Bcl-2 in granulation tissue of diabetic rats during wound healing]. |
| 662 | 18191076 | Constant high glucose levels increased p47-phox, p67-phox, and p22-phox expression [components of the Nicotinamide adenine dinucleotide phosphate [NAD(P)H] oxidase complex]; endothelial nitric oxide synthase, nitric oxide, and O(2)(-) production; nitrotyrosine, 8-hydroxy-2'-deoxyguanosine, and caspase-3 expression; and reduced Bcl-2 expression. |
| 663 | 18220582 | The anti-apoptotic action of HGF was due to bcl-2-upregulation and the phosphatidylinositol 3-kinase pathway, which is involved in Akt activation. |
| 664 | 18220582 | NADPH oxidase can be activated in hyperglycemia through the protein kinase C pathway. |
| 665 | 18220582 | From the viewpoint of these molecular mechanisms, HMG-CoA reductase inhibitors (statins) might inhibit the high glucose-induced NADPH oxidase activation through inhibition of Rac activity and finally prevent the increase in ROS production in diabetes. |
| 666 | 18225590 | The expression of EGFR, erbB2, erbB3, FGFR-2, FGFR-3, c-myc, N-ras, ets-1, H-ras, c-fos and c-jun, the tumor suppressor genes p53 and p16, apoptosis markers Bax and Bcl-2, and the cell proliferation marker Ki-67 in the sequential stages of rat oral oncogenesis was investigated. |
| 667 | 18225590 | Diabetes seems to promote the activation of the Ras/Raf/MAPK signal transduction pathway mainly by induction of erbB2 and erbB3 receptors, leading to increased cell proliferation, while there was no difference in apoptosis levels during oncogenesis. |
| 668 | 18387670 | We measured mRNA levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), Bcl-2 associated X protein (Bax), B-cell lymphoma protein (Bcl-2), tumor suppressor protein-53 (p53), paired box protein-3 (Pax-3) and vascular endothelial growth factor-A (Vegf-A). |
| 669 | 18387670 | Moreover, we found that maternal diabetes causes decreased expression of genes involved in the oxidative stress defense system (CuZnSOD in non-malformed D11 embryos, MnSOD at all gestational time points, ECSOD and Gpx-1 at GD11-GD15, CAT and Gpx-2 at GD15), decreased expression of Pax-3 at GD11, and increased expression of Vegf-A at all gestational time points. |
| 670 | 18396130 | BAD, a proapoptotic member of the Bcl-2 family of proteins, is regulated by phosphorylation. |
| 671 | 18396130 | A recent study (Danial et al., 2008) suggests a phosphorylation-state-dependent bifunctional role of BAD in the regulation of glucose-stimulated insulin secretion and beta cell mass. |
| 672 | 18414053 | Resveratrol has also been shown to activate various transcription factor (e.g; NFkappaB, STAT3, HIF-1alpha, beta-catenin and PPAR-gamma), suppress the expression of antiapoptotic gene products (e.g; Bcl-2, Bcl-X(L), XIAP and survivin), inhibit protein kinases (e.g; src, PI3K, JNK, and AKT), induce antioxidant enzymes (e,g; catalase, superoxide dismutase and hemoxygenase-1), suppress the expression of inflammatory biomarkers (e.g., TNF, COX-2, iNOS, and CRP), inhibit the expression of angiogenic and metastatic gene products (e.g., MMPs, VEGF, cathepsin D, and ICAM-1), and modulate cell cycle regulatory genes (e.g., p53, Rb, PTEN, cyclins and CDKs). |
| 673 | 18418439 | To assess the level of myocardial reactive oxygen species, we measured malondialdehyde, a surrogate marker of oxidative stress, which was increased in the hearts of NTG and Gsalpha diabetic mice. |
| 674 | 18418439 | In addition, chronic hyperglycemia also increased the activity of catalase and superoxide dismutase in the hearts of NTG and Gsalpha diabetic mice. |
| 675 | 18418439 | Hearts of NTG diabetic mice, but not Gsalpha mice, showed increased expression of proapoptosis Bax, downregulation in Bcl2, and an increase in the Bax/Bcl2 ratio. |
| 676 | 18468463 | The dynamics of CD4(+) effector T cells (Teff cells) and CD4(+)Foxp3(+) regulatory T cells (Treg cells) during diabetes progression in nonobese diabetic mice was investigated to determine whether an imbalance of Treg cells and Teff cells contributes to the development of type 1 diabetes. |
| 677 | 18468463 | Intra-islet Treg cells expressed reduced amounts of CD25 and Bcl-2, suggesting that their decline was due to increased apoptosis. |
| 678 | 18481334 | The data indicated that methylglyoxal induced mouse Neuro-2A neuroblastoma (Neuro-2A) cell apoptosis via alternation of mitochondria membrane potential and Bax/Bcl-2 ratio, activation of caspase-3, and cleavage of poly (ADP-ribose) polymerase. |
| 679 | 18481334 | Furthermore, the results demonstrated that activation of mitogen-activated protein kinase signal pathways (JNK and p38) participated in the methylglyoxal-induced Neuro-2A cell apoptosis process. |
| 680 | 18488169 | Rats were euthanized on Day 87, and hippocampi were excised for visual (light and transmission electron microscopic) and immunochemical (Western blot; immunohistochemical) assessments of the CA1 subfield for apoptosis and expression of regulatory proteins Bcl-2 and Bax. |
| 681 | 18488169 | Treatment responses to all the parameters examined (body weight, plasma glucose, Y-maze error rates, pyramidal cell ultrastructure, proportions of apoptotic cells, levels of expression of Bcl-2 and Bax, and survivability of neuronal cells) were identical: there were highly significant differences between DM and CON groups (P<0.001), but the effects were significantly moderated (P<0.01) in DM+A compared with DM. |
| 682 | 18488169 | These findings confirm the association of apoptosis with the encephalopathic effects of diabetes mellitus, and suggest a major role of the expression levels of Bcl-2 and Bax in the regulation of apoptotic cell death. |
| 683 | 18488169 | All of the results suggest that aucubin could effectively inhibit apoptosis by modulating the expressions of Bcl-2 and Bax genes. |
| 684 | 18488169 | Rats were euthanized on Day 87, and hippocampi were excised for visual (light and transmission electron microscopic) and immunochemical (Western blot; immunohistochemical) assessments of the CA1 subfield for apoptosis and expression of regulatory proteins Bcl-2 and Bax. |
| 685 | 18488169 | Treatment responses to all the parameters examined (body weight, plasma glucose, Y-maze error rates, pyramidal cell ultrastructure, proportions of apoptotic cells, levels of expression of Bcl-2 and Bax, and survivability of neuronal cells) were identical: there were highly significant differences between DM and CON groups (P<0.001), but the effects were significantly moderated (P<0.01) in DM+A compared with DM. |
| 686 | 18488169 | These findings confirm the association of apoptosis with the encephalopathic effects of diabetes mellitus, and suggest a major role of the expression levels of Bcl-2 and Bax in the regulation of apoptotic cell death. |
| 687 | 18488169 | All of the results suggest that aucubin could effectively inhibit apoptosis by modulating the expressions of Bcl-2 and Bax genes. |
| 688 | 18488169 | Rats were euthanized on Day 87, and hippocampi were excised for visual (light and transmission electron microscopic) and immunochemical (Western blot; immunohistochemical) assessments of the CA1 subfield for apoptosis and expression of regulatory proteins Bcl-2 and Bax. |
| 689 | 18488169 | Treatment responses to all the parameters examined (body weight, plasma glucose, Y-maze error rates, pyramidal cell ultrastructure, proportions of apoptotic cells, levels of expression of Bcl-2 and Bax, and survivability of neuronal cells) were identical: there were highly significant differences between DM and CON groups (P<0.001), but the effects were significantly moderated (P<0.01) in DM+A compared with DM. |
| 690 | 18488169 | These findings confirm the association of apoptosis with the encephalopathic effects of diabetes mellitus, and suggest a major role of the expression levels of Bcl-2 and Bax in the regulation of apoptotic cell death. |
| 691 | 18488169 | All of the results suggest that aucubin could effectively inhibit apoptosis by modulating the expressions of Bcl-2 and Bax genes. |
| 692 | 18488169 | Rats were euthanized on Day 87, and hippocampi were excised for visual (light and transmission electron microscopic) and immunochemical (Western blot; immunohistochemical) assessments of the CA1 subfield for apoptosis and expression of regulatory proteins Bcl-2 and Bax. |
| 693 | 18488169 | Treatment responses to all the parameters examined (body weight, plasma glucose, Y-maze error rates, pyramidal cell ultrastructure, proportions of apoptotic cells, levels of expression of Bcl-2 and Bax, and survivability of neuronal cells) were identical: there were highly significant differences between DM and CON groups (P<0.001), but the effects were significantly moderated (P<0.01) in DM+A compared with DM. |
| 694 | 18488169 | These findings confirm the association of apoptosis with the encephalopathic effects of diabetes mellitus, and suggest a major role of the expression levels of Bcl-2 and Bax in the regulation of apoptotic cell death. |
| 695 | 18488169 | All of the results suggest that aucubin could effectively inhibit apoptosis by modulating the expressions of Bcl-2 and Bax genes. |
| 696 | 18506358 | Apoptosis was assessed by TUNEL assay, nitrotyrosine and poly(ADP-ribose) by immunocytochemistry, and Bax and Bcl-2 expression by Western blot analyses. |
| 697 | 18506358 | Antiapoptotic effect of fidarestat in high glucose-exposed retinal pericytes was not associated with the inhibition of Bax or increase in Bcl-2 expression. |
| 698 | 18506358 | Apoptosis was assessed by TUNEL assay, nitrotyrosine and poly(ADP-ribose) by immunocytochemistry, and Bax and Bcl-2 expression by Western blot analyses. |
| 699 | 18506358 | Antiapoptotic effect of fidarestat in high glucose-exposed retinal pericytes was not associated with the inhibition of Bax or increase in Bcl-2 expression. |
| 700 | 18524857 | Under diabetic conditions, Bcl-2 protein expression was decreased, whereas cleaved caspase-3 protein expression was increased (P < 0.05), and these changes were inhibited by FR167653 treatment. |
| 701 | 18626456 | Four samples were subjected to Immunohistochemistry (IHC) staining using antibodies to T cell marker (CD3), B cell marker (CD20), anti apoptotic markers (bcl-2) and tumour suppressor gene marker p53. |
| 702 | 18753253 | The GTPase Ras-proximate-1 (Rap1b) is upregulated in the hyperglycemic state and is known to increase B-Raf, an antiapoptotic effector protein. |
| 703 | 18753253 | In the kidneys of diabetic mice, apoptotic tubular cells and dysmorphic mitochondria were observed, Bcl-2 expression was decreased, and Bax expression was increased. |
| 704 | 18753253 | In vitro, high extracellular glucose led to decreased Bcl-2 expression, reduced Rap1b GTPase activity, and increased levels of both Bax and GTPase activating protein in a proximal tubular cell line (HK-2). |
| 705 | 18753253 | Furthermore, the BH4 domain of Bcl-2 was found to be required for successful protein-protein interaction between Bcl-2 and Rap1b. |
| 706 | 18753253 | The GTPase Ras-proximate-1 (Rap1b) is upregulated in the hyperglycemic state and is known to increase B-Raf, an antiapoptotic effector protein. |
| 707 | 18753253 | In the kidneys of diabetic mice, apoptotic tubular cells and dysmorphic mitochondria were observed, Bcl-2 expression was decreased, and Bax expression was increased. |
| 708 | 18753253 | In vitro, high extracellular glucose led to decreased Bcl-2 expression, reduced Rap1b GTPase activity, and increased levels of both Bax and GTPase activating protein in a proximal tubular cell line (HK-2). |
| 709 | 18753253 | Furthermore, the BH4 domain of Bcl-2 was found to be required for successful protein-protein interaction between Bcl-2 and Rap1b. |
| 710 | 18753253 | The GTPase Ras-proximate-1 (Rap1b) is upregulated in the hyperglycemic state and is known to increase B-Raf, an antiapoptotic effector protein. |
| 711 | 18753253 | In the kidneys of diabetic mice, apoptotic tubular cells and dysmorphic mitochondria were observed, Bcl-2 expression was decreased, and Bax expression was increased. |
| 712 | 18753253 | In vitro, high extracellular glucose led to decreased Bcl-2 expression, reduced Rap1b GTPase activity, and increased levels of both Bax and GTPase activating protein in a proximal tubular cell line (HK-2). |
| 713 | 18753253 | Furthermore, the BH4 domain of Bcl-2 was found to be required for successful protein-protein interaction between Bcl-2 and Rap1b. |
| 714 | 18758938 | Evaluation of insulin and ascorbic acid effects on expression of Bcl-2 family proteins and caspase-3 activity in hippocampus of STZ-induced diabetic rats. |
| 715 | 18763577 | To reveal insulin-expressing, proliferating, Treg-cells, iNOS(+)-cells and Bcl-2(+)-cells, the immunohistochemical methods of direct and indirect immunofluorescence with monoclonal antibodies to insulin, PCNA, CD-25 antigen. |
| 716 | 18763577 | Bcl-2 and iNOS of rat were used. |
| 717 | 18763577 | It was established that NNLA administration to rats with EDM has more pronounced effect in comparison with L-arginine administration, demonstrating an increase in the number of Treg-cells, insulin-expressing and proliferating thymocytes and a decrease in the density of iNOS(+)- and Bcl-2(+)-cells population. |
| 718 | 18763577 | To reveal insulin-expressing, proliferating, Treg-cells, iNOS(+)-cells and Bcl-2(+)-cells, the immunohistochemical methods of direct and indirect immunofluorescence with monoclonal antibodies to insulin, PCNA, CD-25 antigen. |
| 719 | 18763577 | Bcl-2 and iNOS of rat were used. |
| 720 | 18763577 | It was established that NNLA administration to rats with EDM has more pronounced effect in comparison with L-arginine administration, demonstrating an increase in the number of Treg-cells, insulin-expressing and proliferating thymocytes and a decrease in the density of iNOS(+)- and Bcl-2(+)-cells population. |
| 721 | 18763577 | To reveal insulin-expressing, proliferating, Treg-cells, iNOS(+)-cells and Bcl-2(+)-cells, the immunohistochemical methods of direct and indirect immunofluorescence with monoclonal antibodies to insulin, PCNA, CD-25 antigen. |
| 722 | 18763577 | Bcl-2 and iNOS of rat were used. |
| 723 | 18763577 | It was established that NNLA administration to rats with EDM has more pronounced effect in comparison with L-arginine administration, demonstrating an increase in the number of Treg-cells, insulin-expressing and proliferating thymocytes and a decrease in the density of iNOS(+)- and Bcl-2(+)-cells population. |
| 724 | 18813861 | Therefore, we directly investigated exercise training to determine whether it was able to ameliorate the molecular pathogenic phenotypes in the brain using a neuron-specific enolase (NSE)/Swedish mutation of amyloid precursor protein (APPsw) transgenic (Tg) mice as a novel AD model. |
| 725 | 18813861 | The results indicated (i) that amyloid beta-42 (Abeta-42) peptides were significantly decreased in the NSE/APPsw Tg mice following exercise training; (ii) that exercise training inhibited the apoptotic biochemical cascades, including cytochrome c, caspase-9, caspase-3 and Bax; (iii) that the glucose transporter-1 (GLUT-1) and brain-derived neurotrophic factor (BDNF) proteins induced by exercise training protected the neurons from injury by inducing the concomitant expression of genes that encode proteins such as superoxide dismutase-1 (SOD-1), catalase and Bcl-2, which suppress oxidative stress and excitotoxic injury; (iv) that heat-shock protein-70 (HSP-70) and glucose-regulated protein-78 (GRP-78) were significantly increased in the exercise (EXE) group when compared to the sedentary (SED) group, and that these proteins may benefit the brain by making it more resistant to stress-induced neuron cell damage; (v) and that exercise training contributed to the restoration of normal levels of serum total cholesterol, insulin and glucose. |
| 726 | 18832793 | We analyzed the changes in neurological severity scores, infarct volume, number of apoptotic neurons, and the expression of G-CSF receptor, phosphorylated signal transducer and activator of transcription 3 (pSTAT3), cellular inhibitor of apoptosis protein 2 (cIAP2), Bcl-2, and Bax in the brain tissue. |
| 727 | 18832793 | Bax is a pro-apoptotic member of the Bcl-2 protein family. |
| 728 | 18832793 | The G-CSF also increased the expression of pSTAT3, Bcl-2, and cIAP2 proteins as well as Bcl-2 mRNA, but inhibited Bax protein expression in the brain. |
| 729 | 18832793 | We analyzed the changes in neurological severity scores, infarct volume, number of apoptotic neurons, and the expression of G-CSF receptor, phosphorylated signal transducer and activator of transcription 3 (pSTAT3), cellular inhibitor of apoptosis protein 2 (cIAP2), Bcl-2, and Bax in the brain tissue. |
| 730 | 18832793 | Bax is a pro-apoptotic member of the Bcl-2 protein family. |
| 731 | 18832793 | The G-CSF also increased the expression of pSTAT3, Bcl-2, and cIAP2 proteins as well as Bcl-2 mRNA, but inhibited Bax protein expression in the brain. |
| 732 | 18832793 | We analyzed the changes in neurological severity scores, infarct volume, number of apoptotic neurons, and the expression of G-CSF receptor, phosphorylated signal transducer and activator of transcription 3 (pSTAT3), cellular inhibitor of apoptosis protein 2 (cIAP2), Bcl-2, and Bax in the brain tissue. |
| 733 | 18832793 | Bax is a pro-apoptotic member of the Bcl-2 protein family. |
| 734 | 18832793 | The G-CSF also increased the expression of pSTAT3, Bcl-2, and cIAP2 proteins as well as Bcl-2 mRNA, but inhibited Bax protein expression in the brain. |
| 735 | 18840766 | However, the role of Bax and Bcl-2 in regulating palmitate-induced apoptosis has not been well studied. |
| 736 | 18840766 | Therefore, the purpose of this study was to determine whether palmitate-induced apoptosis in C(2)C(12) myotubes is dependent on Bax to Bcl-2 binding. |
| 737 | 18840766 | An additional purpose of this study was to determine whether the changes in Bax to Bcl-2 binding corresponded to decreases in Akt signaling in palmitate-treated myoblasts. |
| 738 | 18840766 | Bax to Bcl-2 binding was determined through a coimmunoprecipitation assay that was performed in myotubes after 2 h of serum starvation, followed by 10 min of serum reintroduction. |
| 739 | 18840766 | This experiment evaluated whether temporal Akt activity coincided with Bax to Bcl-2 binding. |
| 740 | 18840766 | Palmitate treatment increased apoptosis in C(2)C(12) myotubes as shown by a twofold increase in DNA fragmentation, an approximately fivefold increase in caspase-3 activity, and a 2.5-fold increase in caspase-9 activity. |
| 741 | 18840766 | In addition, there was a fourfold reduction in Bax to Bcl-2 binding with palmitate treatment, which mirrored the reduction in Akt(Ser473) phosphorylation. |
| 742 | 18840766 | However, the role of Bax and Bcl-2 in regulating palmitate-induced apoptosis has not been well studied. |
| 743 | 18840766 | Therefore, the purpose of this study was to determine whether palmitate-induced apoptosis in C(2)C(12) myotubes is dependent on Bax to Bcl-2 binding. |
| 744 | 18840766 | An additional purpose of this study was to determine whether the changes in Bax to Bcl-2 binding corresponded to decreases in Akt signaling in palmitate-treated myoblasts. |
| 745 | 18840766 | Bax to Bcl-2 binding was determined through a coimmunoprecipitation assay that was performed in myotubes after 2 h of serum starvation, followed by 10 min of serum reintroduction. |
| 746 | 18840766 | This experiment evaluated whether temporal Akt activity coincided with Bax to Bcl-2 binding. |
| 747 | 18840766 | Palmitate treatment increased apoptosis in C(2)C(12) myotubes as shown by a twofold increase in DNA fragmentation, an approximately fivefold increase in caspase-3 activity, and a 2.5-fold increase in caspase-9 activity. |
| 748 | 18840766 | In addition, there was a fourfold reduction in Bax to Bcl-2 binding with palmitate treatment, which mirrored the reduction in Akt(Ser473) phosphorylation. |
| 749 | 18840766 | However, the role of Bax and Bcl-2 in regulating palmitate-induced apoptosis has not been well studied. |
| 750 | 18840766 | Therefore, the purpose of this study was to determine whether palmitate-induced apoptosis in C(2)C(12) myotubes is dependent on Bax to Bcl-2 binding. |
| 751 | 18840766 | An additional purpose of this study was to determine whether the changes in Bax to Bcl-2 binding corresponded to decreases in Akt signaling in palmitate-treated myoblasts. |
| 752 | 18840766 | Bax to Bcl-2 binding was determined through a coimmunoprecipitation assay that was performed in myotubes after 2 h of serum starvation, followed by 10 min of serum reintroduction. |
| 753 | 18840766 | This experiment evaluated whether temporal Akt activity coincided with Bax to Bcl-2 binding. |
| 754 | 18840766 | Palmitate treatment increased apoptosis in C(2)C(12) myotubes as shown by a twofold increase in DNA fragmentation, an approximately fivefold increase in caspase-3 activity, and a 2.5-fold increase in caspase-9 activity. |
| 755 | 18840766 | In addition, there was a fourfold reduction in Bax to Bcl-2 binding with palmitate treatment, which mirrored the reduction in Akt(Ser473) phosphorylation. |
| 756 | 18840766 | However, the role of Bax and Bcl-2 in regulating palmitate-induced apoptosis has not been well studied. |
| 757 | 18840766 | Therefore, the purpose of this study was to determine whether palmitate-induced apoptosis in C(2)C(12) myotubes is dependent on Bax to Bcl-2 binding. |
| 758 | 18840766 | An additional purpose of this study was to determine whether the changes in Bax to Bcl-2 binding corresponded to decreases in Akt signaling in palmitate-treated myoblasts. |
| 759 | 18840766 | Bax to Bcl-2 binding was determined through a coimmunoprecipitation assay that was performed in myotubes after 2 h of serum starvation, followed by 10 min of serum reintroduction. |
| 760 | 18840766 | This experiment evaluated whether temporal Akt activity coincided with Bax to Bcl-2 binding. |
| 761 | 18840766 | Palmitate treatment increased apoptosis in C(2)C(12) myotubes as shown by a twofold increase in DNA fragmentation, an approximately fivefold increase in caspase-3 activity, and a 2.5-fold increase in caspase-9 activity. |
| 762 | 18840766 | In addition, there was a fourfold reduction in Bax to Bcl-2 binding with palmitate treatment, which mirrored the reduction in Akt(Ser473) phosphorylation. |
| 763 | 18840766 | However, the role of Bax and Bcl-2 in regulating palmitate-induced apoptosis has not been well studied. |
| 764 | 18840766 | Therefore, the purpose of this study was to determine whether palmitate-induced apoptosis in C(2)C(12) myotubes is dependent on Bax to Bcl-2 binding. |
| 765 | 18840766 | An additional purpose of this study was to determine whether the changes in Bax to Bcl-2 binding corresponded to decreases in Akt signaling in palmitate-treated myoblasts. |
| 766 | 18840766 | Bax to Bcl-2 binding was determined through a coimmunoprecipitation assay that was performed in myotubes after 2 h of serum starvation, followed by 10 min of serum reintroduction. |
| 767 | 18840766 | This experiment evaluated whether temporal Akt activity coincided with Bax to Bcl-2 binding. |
| 768 | 18840766 | Palmitate treatment increased apoptosis in C(2)C(12) myotubes as shown by a twofold increase in DNA fragmentation, an approximately fivefold increase in caspase-3 activity, and a 2.5-fold increase in caspase-9 activity. |
| 769 | 18840766 | In addition, there was a fourfold reduction in Bax to Bcl-2 binding with palmitate treatment, which mirrored the reduction in Akt(Ser473) phosphorylation. |
| 770 | 18840766 | However, the role of Bax and Bcl-2 in regulating palmitate-induced apoptosis has not been well studied. |
| 771 | 18840766 | Therefore, the purpose of this study was to determine whether palmitate-induced apoptosis in C(2)C(12) myotubes is dependent on Bax to Bcl-2 binding. |
| 772 | 18840766 | An additional purpose of this study was to determine whether the changes in Bax to Bcl-2 binding corresponded to decreases in Akt signaling in palmitate-treated myoblasts. |
| 773 | 18840766 | Bax to Bcl-2 binding was determined through a coimmunoprecipitation assay that was performed in myotubes after 2 h of serum starvation, followed by 10 min of serum reintroduction. |
| 774 | 18840766 | This experiment evaluated whether temporal Akt activity coincided with Bax to Bcl-2 binding. |
| 775 | 18840766 | Palmitate treatment increased apoptosis in C(2)C(12) myotubes as shown by a twofold increase in DNA fragmentation, an approximately fivefold increase in caspase-3 activity, and a 2.5-fold increase in caspase-9 activity. |
| 776 | 18840766 | In addition, there was a fourfold reduction in Bax to Bcl-2 binding with palmitate treatment, which mirrored the reduction in Akt(Ser473) phosphorylation. |
| 777 | 18923682 | Evaluation of Bcl-2 family gene expression and Caspase-3 activity in hippocampus STZ-induced diabetic rats. |
| 778 | 18923682 | We assessed the expression of Bcl-2 family members at both mRNA and protein levels as well as the Caspase-3 activity, in order to investigate the occurrence of apoptosis in hippocampus of STZ-induced diabetic rats. |
| 779 | 18923682 | The expressions of Bcl-2, Bcl-x(L), and Bax mRNA and proteins were measured using RT-PCR and western blotting, respectively. |
| 780 | 18923682 | The result showed that mRNA and protein levels of Bcl-2 and Bcl-x(L) were lower in hippocampus of diabetic group than that of the control group, whereas expressions of Bax in hippocampus of diabetic rats were higher than that of controls at both mRNA and protein levels (P < .01). |
| 781 | 18923682 | Therefore, the induction of diabetes is associated with increased ratios of Bax/Bcl-2, Bax/Bcl-x(L), and increased caspase-3 activity in hippocampus which shows that apoptosis is favored in hippocampal region. |
| 782 | 18923682 | Evaluation of Bcl-2 family gene expression and Caspase-3 activity in hippocampus STZ-induced diabetic rats. |
| 783 | 18923682 | We assessed the expression of Bcl-2 family members at both mRNA and protein levels as well as the Caspase-3 activity, in order to investigate the occurrence of apoptosis in hippocampus of STZ-induced diabetic rats. |
| 784 | 18923682 | The expressions of Bcl-2, Bcl-x(L), and Bax mRNA and proteins were measured using RT-PCR and western blotting, respectively. |
| 785 | 18923682 | The result showed that mRNA and protein levels of Bcl-2 and Bcl-x(L) were lower in hippocampus of diabetic group than that of the control group, whereas expressions of Bax in hippocampus of diabetic rats were higher than that of controls at both mRNA and protein levels (P < .01). |
| 786 | 18923682 | Therefore, the induction of diabetes is associated with increased ratios of Bax/Bcl-2, Bax/Bcl-x(L), and increased caspase-3 activity in hippocampus which shows that apoptosis is favored in hippocampal region. |
| 787 | 18923682 | Evaluation of Bcl-2 family gene expression and Caspase-3 activity in hippocampus STZ-induced diabetic rats. |
| 788 | 18923682 | We assessed the expression of Bcl-2 family members at both mRNA and protein levels as well as the Caspase-3 activity, in order to investigate the occurrence of apoptosis in hippocampus of STZ-induced diabetic rats. |
| 789 | 18923682 | The expressions of Bcl-2, Bcl-x(L), and Bax mRNA and proteins were measured using RT-PCR and western blotting, respectively. |
| 790 | 18923682 | The result showed that mRNA and protein levels of Bcl-2 and Bcl-x(L) were lower in hippocampus of diabetic group than that of the control group, whereas expressions of Bax in hippocampus of diabetic rats were higher than that of controls at both mRNA and protein levels (P < .01). |
| 791 | 18923682 | Therefore, the induction of diabetes is associated with increased ratios of Bax/Bcl-2, Bax/Bcl-x(L), and increased caspase-3 activity in hippocampus which shows that apoptosis is favored in hippocampal region. |
| 792 | 18923682 | Evaluation of Bcl-2 family gene expression and Caspase-3 activity in hippocampus STZ-induced diabetic rats. |
| 793 | 18923682 | We assessed the expression of Bcl-2 family members at both mRNA and protein levels as well as the Caspase-3 activity, in order to investigate the occurrence of apoptosis in hippocampus of STZ-induced diabetic rats. |
| 794 | 18923682 | The expressions of Bcl-2, Bcl-x(L), and Bax mRNA and proteins were measured using RT-PCR and western blotting, respectively. |
| 795 | 18923682 | The result showed that mRNA and protein levels of Bcl-2 and Bcl-x(L) were lower in hippocampus of diabetic group than that of the control group, whereas expressions of Bax in hippocampus of diabetic rats were higher than that of controls at both mRNA and protein levels (P < .01). |
| 796 | 18923682 | Therefore, the induction of diabetes is associated with increased ratios of Bax/Bcl-2, Bax/Bcl-x(L), and increased caspase-3 activity in hippocampus which shows that apoptosis is favored in hippocampal region. |
| 797 | 18923682 | Evaluation of Bcl-2 family gene expression and Caspase-3 activity in hippocampus STZ-induced diabetic rats. |
| 798 | 18923682 | We assessed the expression of Bcl-2 family members at both mRNA and protein levels as well as the Caspase-3 activity, in order to investigate the occurrence of apoptosis in hippocampus of STZ-induced diabetic rats. |
| 799 | 18923682 | The expressions of Bcl-2, Bcl-x(L), and Bax mRNA and proteins were measured using RT-PCR and western blotting, respectively. |
| 800 | 18923682 | The result showed that mRNA and protein levels of Bcl-2 and Bcl-x(L) were lower in hippocampus of diabetic group than that of the control group, whereas expressions of Bax in hippocampus of diabetic rats were higher than that of controls at both mRNA and protein levels (P < .01). |
| 801 | 18923682 | Therefore, the induction of diabetes is associated with increased ratios of Bax/Bcl-2, Bax/Bcl-x(L), and increased caspase-3 activity in hippocampus which shows that apoptosis is favored in hippocampal region. |
| 802 | 19164757 | Like bortezomib, EerI-induced cytotoxicity requires the up-regulation of the Bcl-2 homology3 (BH3)-only pro-apoptotic protein NOXA. |
| 803 | 19164757 | First, these agents elicit an integrated stress response program at the ER to activate the CREB/ATF transcription factors ATF3 and ATF4. |
| 804 | 19164757 | We show that ATF3 and ATF4 form a complex capable of binding to the NOXA promoter, which is required for NOXA activation. |
| 805 | 19164757 | Second, EerI and bortezomib also block ubiquitination of histone H2A to relieve its inhibition on NOXA transcription. |
| 806 | 19177839 | We studied the expression of a set of selected genes involved in apoptosis (Bcl2, Bclx(L), Bax, Bad, Bid, and CHOP), cytokine defense, (SOCS-1 and SOCS-3), or free radical protection (Hmox1, Cu/Zn-SOD, Mn-SOD, and Hsp70). |
| 807 | 19177839 | The expression of proapoptotic genes Bid and CHOP, as well as protective genes Bclx(L), Socs1, Socs3, Hmox1, and MnSod, was maximally increased 1 day after transplantation, and in most cases it remained increased 7 days later, indicating the presence of a protective response against cell damage. |
| 808 | 19177839 | In contrast, the expression of Bcl2, Bax, Bad, Cu/ZnSod, and Hsp70 genes did not change. |
| 809 | 19177839 | We studied the expression of a set of selected genes involved in apoptosis (Bcl2, Bclx(L), Bax, Bad, Bid, and CHOP), cytokine defense, (SOCS-1 and SOCS-3), or free radical protection (Hmox1, Cu/Zn-SOD, Mn-SOD, and Hsp70). |
| 810 | 19177839 | The expression of proapoptotic genes Bid and CHOP, as well as protective genes Bclx(L), Socs1, Socs3, Hmox1, and MnSod, was maximally increased 1 day after transplantation, and in most cases it remained increased 7 days later, indicating the presence of a protective response against cell damage. |
| 811 | 19177839 | In contrast, the expression of Bcl2, Bax, Bad, Cu/ZnSod, and Hsp70 genes did not change. |
| 812 | 19209227 | Previous gain-of-function studies in the RIP1-Tag2 model of pancreatic islet carcinogenesis, involving uniform or focal/temporal over-expression of Bcl-x(L), demonstrated accelerated tumor formation and growth. |
| 813 | 19209227 | Other anti-apoptotic Bcl-2 family members were expressed but not substantively altered at the mRNA level in the Bcl-x-null tumors, suggestive of redundancy without compensatory transcriptional up-regulation. |
| 814 | 19279000 | Glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 modulate beta-cell chromatin structure. |
| 815 | 19279000 | In the present study, we examined whether nuclear actions of the incretin hormones, glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1, involve modulation of beta-cell chromatin structure. |
| 816 | 19279000 | Stimulation of INS-1(832/13) beta-cells or dispersed mouse islets with glucose-dependent insulinotropic polypeptide or glucagon-like peptide-1 resulted in the post-translational modification of core H3 histones, through acetylation and phosphorylation. |
| 817 | 19279000 | Subsequent studies demonstrated that incretin-mediated histone H3 modifications involved activation of protein kinase A, p42/44 mitogen-activated protein kinase (MAPK), and p38 MAPK signaling modules, resulting in the activation of mitogen- and stress-activated kinase-1. |
| 818 | 19279000 | Incretin-activated CREB-related Bcl-2 transcription was greatly reduced by a histone acetyltransferase inhibitor, demonstrating the functional importance of histone H3 modification. |
| 819 | 19330083 | Upregulation of heme oxygenase-1 combined with increased adiponectin lowers blood pressure in diabetic spontaneously hypertensive rats through a reduction in endothelial cell dysfunction, apoptosis and oxidative stress. |
| 820 | 19330083 | Treatment with SnCl(2) not only attenuated the increase of blood pressure (p<0.01), but also increased HO-1 protein content, HO activity and plasma adiponectin levels, decreased the levels of superoxide and 3-nitrotyrosine (NT), respectively. |
| 821 | 19330083 | Reduction in oxidative stress resulted in the increased expression of Bcl-2 and AKT with a concomitant reduction in circulating endothelial cells (CEC) in the peripheral blood (p<0.005) and an improvement of femoral reactivity (response to acetylcholine). |
| 822 | 19330083 | Thus induction of HO-1 accompanied with increased plasma adiponectin levels in diabetic hypertensive rats alters the phenotype through a reduction in oxidative stress, thereby permitting endothelial cells to maintain an anti-apoptotic environment and the restoration of endothelial responses thus preventing hypertension. |
| 823 | 19393315 | Genistein and daidzein upregulated the estrogen receptor ERbeta and increased Bcl-2 expression. |
| 824 | 19393315 | Moreover, inhibition of the PI3K and Rho A/Rho kinase pathways by wortmannin and Y-27632 altered the effects of genistein and daidzein on cell survival. |
| 825 | 19393315 | We conclude that oxidative stress-induced apoptosis and cell proliferation inhibition can be prevented by soy isoflavones via the regulation of ERbeta and Bcl-2/Bax expression and modulation of cell survival signaling, such as the PI3K pathway. |
| 826 | 19393315 | Genistein and daidzein upregulated the estrogen receptor ERbeta and increased Bcl-2 expression. |
| 827 | 19393315 | Moreover, inhibition of the PI3K and Rho A/Rho kinase pathways by wortmannin and Y-27632 altered the effects of genistein and daidzein on cell survival. |
| 828 | 19393315 | We conclude that oxidative stress-induced apoptosis and cell proliferation inhibition can be prevented by soy isoflavones via the regulation of ERbeta and Bcl-2/Bax expression and modulation of cell survival signaling, such as the PI3K pathway. |
| 829 | 19411758 | Bim, the B cell lymphoma 2-interacting (Bcl2-interacting) mediator, maintains immunological tolerance by deleting autoreactive lymphocytes through apoptosis. |
| 830 | 19411758 | Upon T cell receptor activation, Bim-deficient T cells exhibited severe defects in both calcium release and dephosphorylation of nuclear factor of activated T cells (NFAT) but maintained normal levels of activation of NF-kappaB and MAPKs. |
| 831 | 19411758 | The defective calcium signaling in Bim-deficient T cells was associated with a significant increase in the formation of an inhibitory complex containing Bcl2 and the inositol triphosphate receptor (IP3R). |
| 832 | 19411758 | Thus, in addition to mediating the death of autoreactive T cells, Bim also controlled T cell activation through the IP3R/calcium/NFAT pathway. |
| 833 | 19411758 | Bim, the B cell lymphoma 2-interacting (Bcl2-interacting) mediator, maintains immunological tolerance by deleting autoreactive lymphocytes through apoptosis. |
| 834 | 19411758 | Upon T cell receptor activation, Bim-deficient T cells exhibited severe defects in both calcium release and dephosphorylation of nuclear factor of activated T cells (NFAT) but maintained normal levels of activation of NF-kappaB and MAPKs. |
| 835 | 19411758 | The defective calcium signaling in Bim-deficient T cells was associated with a significant increase in the formation of an inhibitory complex containing Bcl2 and the inositol triphosphate receptor (IP3R). |
| 836 | 19411758 | Thus, in addition to mediating the death of autoreactive T cells, Bim also controlled T cell activation through the IP3R/calcium/NFAT pathway. |
| 837 | 19455054 | The level of cytochrome c expression and caspase 3 activation was also reduced. |
| 838 | 19455054 | BHE elevated antiapoptotic proteins Bcl-2 and heme oxygenase-1 and stimulated the phosphorylation of survival protein Akt simultaneously decreasing the apoptotic proteins Bax and Src. |
| 839 | 19455054 | In addition, BHE enhanced the protein expression of peroxisome proliferator-activated receptor-gamma, peroxisome proliferator-activated receptor-delta, and Glut-4, probably revealing the antiobese and antidiabetic potential of BHE. |
| 840 | 19463916 | Twenty-three retinal genes, mainly from TNF ligand and receptor, caspase, Bcl-2 and death domain subfamilies that were upregulated by least a two-fold in PC rats remain upregulated after reversal of hyperglycemia. |
| 841 | 19467786 | We previously reported that high glucose can induce apoptosis in PC12 cells, as evidenced by DNA fragmentation and high Bax/Bcl-2 ratio. |
| 842 | 19467786 | The present study examined the involvement of caspase-3, the executioner, and two initiators of apoptosis, caspase-8 and caspase-9, during high glucose-induced apoptosis in PC12 cells, a neuronal cell line. |
| 843 | 19540304 | Ghrelin did not modify body weight or serum glucose, leptin or adiponectin, but increased total ghrelin (P<0.05), IGF-I (P<0.01) and prolactin (P<0.01) levels. |
| 844 | 19540304 | Ghrelin decreased cell death, iNOS and active caspase-8 (P<0.05) and increased prolactin (P<0.05), Bcl-2 (P<0.01) and Hsp70 (P<0.05) content in the pituitary. |
| 845 | 19540304 | In conclusion, ghrelin prevents diabetes-induced death of lactotrophs, decreasing caspase-8 activation and iNOS content and increasing anti-apoptotic pathways such as pituitary Bcl-2 and Hsp70 and serum IGF-I concentrations. |
| 846 | 19540304 | Ghrelin did not modify body weight or serum glucose, leptin or adiponectin, but increased total ghrelin (P<0.05), IGF-I (P<0.01) and prolactin (P<0.01) levels. |
| 847 | 19540304 | Ghrelin decreased cell death, iNOS and active caspase-8 (P<0.05) and increased prolactin (P<0.05), Bcl-2 (P<0.01) and Hsp70 (P<0.05) content in the pituitary. |
| 848 | 19540304 | In conclusion, ghrelin prevents diabetes-induced death of lactotrophs, decreasing caspase-8 activation and iNOS content and increasing anti-apoptotic pathways such as pituitary Bcl-2 and Hsp70 and serum IGF-I concentrations. |
| 849 | 19556421 | To clarify whether the molecular pathways elicited by NO and ER Ca(2+) depletion differ, we here compare the direct effects of NO, in the form of the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP), with the effects of SERCA2 inhibitor thapsigargin (TG) on MAPK, nuclear factor kappaB (NFkappaB), Bcl-2 proteins, ER stress, and apoptosis. |
| 850 | 19556421 | Both TG and SNAP induced activation of the proapoptotic transcription factor CCAAT/enhancer-binding protein homologous protein (CHOP). |
| 851 | 19556421 | Inhibition of NFkappaB or the Bcl-2 family member Bax pathways protected beta-cells against TG- but not SNAP-induced beta-cell death. |
| 852 | 19556421 | To clarify whether the molecular pathways elicited by NO and ER Ca(2+) depletion differ, we here compare the direct effects of NO, in the form of the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP), with the effects of SERCA2 inhibitor thapsigargin (TG) on MAPK, nuclear factor kappaB (NFkappaB), Bcl-2 proteins, ER stress, and apoptosis. |
| 853 | 19556421 | Both TG and SNAP induced activation of the proapoptotic transcription factor CCAAT/enhancer-binding protein homologous protein (CHOP). |
| 854 | 19556421 | Inhibition of NFkappaB or the Bcl-2 family member Bax pathways protected beta-cells against TG- but not SNAP-induced beta-cell death. |
| 855 | 19610036 | Apoptosis was inferred by caspase-3 protein expression and caspase-3 activity and changes in Bcl-2 mRNA. |
| 856 | 19610036 | RT-PCR was used to analyse PDX-1, insulin and UCP-2 mRNA expression in RINm5F beta-cells and insulin levels were quantified from the cell culture supernatant. |
| 857 | 19610036 | Gallic acid dose-dependently increased insulin secretion in RINm5F beta-cells and upregulated mRNA of PDX-1 and insulin. |
| 858 | 19629134 | Signaling by IL-1beta+IFN-gamma and ER stress converge on DP5/Hrk activation: a novel mechanism for pancreatic beta-cell apoptosis. |
| 859 | 19629134 | We presently show that the cytokines IL-1beta+IFN-gamma and different ER stressors activate the Bcl-2 homology 3 (BH3)-only member death protein 5 (DP5)/harakiri (Hrk) resulting in beta-cell apoptosis. |
| 860 | 19629134 | Chemical ER stress-induced DP5 upregulation is JNK/c-Jun-dependent. |
| 861 | 19629134 | DP5 activation by cytokines also involves JNK/c-Jun phosphorylation and is antagonized by JunB. |
| 862 | 19629134 | Interestingly, cytokine-inducted DP5 expression precedes ER stress: mitochondrial release of cytochrome c and ER stress are actually a consequence of enhanced DP5 activation by cytokine-mediated nitric oxide formation. |
| 863 | 19629134 | These observations contribute to solve two important questions, namely the mechanism by which IL-1beta+IFN-gamma induce beta-cell death and the nature of the downstream signals by which ER stress 'convinces' beta-cells to trigger apoptosis. |
| 864 | 19657327 | HO-1 expression, its activity, the ratio of Bax/Bcl-2 protein, and active caspase-3 fragments were all significantly higher in isolated glomeruli of diabetic rats and in high glucose-treated podocytes. |
| 865 | 19661098 | The lymphoma was positive for CD20, CD10, and BCL6 and negative for BCL2. |
| 866 | 19706988 | Interestingly, insulin I and II, anti-apoptotic bcl-2, and proliferation promoting ERK-1 gene expressions were significantly upregulated in db/m mice. |
| 867 | 19706988 | Expressions of insulin I and II, bcl-2, and ERK-1 gene were increased in db/m mice, but not in m/m fed a high fat diet. |
| 868 | 19706988 | Interestingly, insulin I and II, anti-apoptotic bcl-2, and proliferation promoting ERK-1 gene expressions were significantly upregulated in db/m mice. |
| 869 | 19706988 | Expressions of insulin I and II, bcl-2, and ERK-1 gene were increased in db/m mice, but not in m/m fed a high fat diet. |
| 870 | 19710242 | Aldosterone synthase (CYP11B2) and MCR mRNA and protein expression were determined by real-time PCR and Western blot, respectively, and aldosterone levels by radioimmunoassay. |
| 871 | 19710242 | CYP11B2 and MCR expression were significantly higher in HG-stimulated podocytes and DM glomeruli compared with NG cells and C glomeruli, respectively, along with increased aldosterone levels. |
| 872 | 19710242 | Western blot analysis revealed that cleaved caspase-3 and Bax expression was significantly increased, whereas Bcl-2 expression was significantly decreased in HG-stimulated podocytes and in DM glomeruli. |
| 873 | 19748889 | Suppression of p38 MAPK and JNK via Akt-mediated inhibition of apoptosis signal-regulating kinase 1 constitutes a core component of the beta-cell pro-survival effects of glucose-dependent insulinotropic polypeptide. |
| 874 | 19748889 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion, insulin biosynthesis, and beta-cell proliferation and survival. |
| 875 | 19748889 | In previous studies GIP was shown to promote beta-cell survival by modulating the activity of multiple signaling modules and regulating gene transcription of pro- and anti-apoptotic bcl-2 family proteins. |
| 876 | 19748889 | We have now evaluated the mechanisms by which GIP regulates the dynamic interactions between cytoplasmic bcl-2 family members and the mitochondria in INS-1 cells during apoptosis induced by treatment with staurosporine (STS), an activator of the mitochondria-mediated apoptotic pathway. |
| 877 | 19748889 | STS induced translocation of bad and bimEL, activation of mitochondrial bax, release of mitochondrial cytochrome c, cleavage of caspase-3, and apoptosis. |
| 878 | 19748889 | Using selective enzyme inhibitors, overexpression of dominant-negative Akt, and Akt siRNA, it was demonstrated that GIP promoted beta-cell survival via Akt-dependent suppression of p38 MAPK and JNK and that combined inhibition was sufficient to explain the entire pro-survival responses to GIP during STS treatment. |
| 879 | 19748889 | This signaling pathway also explained the pro-survival effects of GIP on INS-1 cells exposed to two other promoters of stress: thapsigargin (endoplasmic reticulum stress) and etoposide (genotoxic stress). |
| 880 | 19748889 | Importantly, we discovered that GIP suppressed p38 MAPK and JNK via Akt-mediated changes in the phosphorylation state of the apoptosis signal-regulating kinase 1 in INS-1 cells and human islets, resulting in inhibition of its activity. |
| 881 | 19748889 | Inhibition of apoptosis by GIP is therefore mediated via a key pathway involving Akt-dependent inhibition of apoptosis signal-regulating kinase 1, which subsequently prevents the pro-apoptotic actions of p38 MAPK and JNK. |
| 882 | 19748889 | Suppression of p38 MAPK and JNK via Akt-mediated inhibition of apoptosis signal-regulating kinase 1 constitutes a core component of the beta-cell pro-survival effects of glucose-dependent insulinotropic polypeptide. |
| 883 | 19748889 | Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion, insulin biosynthesis, and beta-cell proliferation and survival. |
| 884 | 19748889 | In previous studies GIP was shown to promote beta-cell survival by modulating the activity of multiple signaling modules and regulating gene transcription of pro- and anti-apoptotic bcl-2 family proteins. |
| 885 | 19748889 | We have now evaluated the mechanisms by which GIP regulates the dynamic interactions between cytoplasmic bcl-2 family members and the mitochondria in INS-1 cells during apoptosis induced by treatment with staurosporine (STS), an activator of the mitochondria-mediated apoptotic pathway. |
| 886 | 19748889 | STS induced translocation of bad and bimEL, activation of mitochondrial bax, release of mitochondrial cytochrome c, cleavage of caspase-3, and apoptosis. |
| 887 | 19748889 | Using selective enzyme inhibitors, overexpression of dominant-negative Akt, and Akt siRNA, it was demonstrated that GIP promoted beta-cell survival via Akt-dependent suppression of p38 MAPK and JNK and that combined inhibition was sufficient to explain the entire pro-survival responses to GIP during STS treatment. |
| 888 | 19748889 | This signaling pathway also explained the pro-survival effects of GIP on INS-1 cells exposed to two other promoters of stress: thapsigargin (endoplasmic reticulum stress) and etoposide (genotoxic stress). |
| 889 | 19748889 | Importantly, we discovered that GIP suppressed p38 MAPK and JNK via Akt-mediated changes in the phosphorylation state of the apoptosis signal-regulating kinase 1 in INS-1 cells and human islets, resulting in inhibition of its activity. |
| 890 | 19748889 | Inhibition of apoptosis by GIP is therefore mediated via a key pathway involving Akt-dependent inhibition of apoptosis signal-regulating kinase 1, which subsequently prevents the pro-apoptotic actions of p38 MAPK and JNK. |
| 891 | 19780024 | Expression (RT-PCR and radioligand binding) and functional (calcium mobilization with fura-2AM, and p42/p44MAPK and Akt phosphorylation assays) experiments revealed the presence of functional B2R in pig cerebral microvascular endothelial cells (pCMVEC). |
| 892 | 19780024 | BK treatment coincided with enhanced expression of the cytoprotective proteins COX-2, Bcl-2, and (Cu/Zn)SOD. |
| 893 | 19785000 | The anti-diabetic effect of anthocyanins in streptozotocin-induced diabetic rats through glucose transporter 4 regulation and prevention of insulin resistance and pancreatic apoptosis. |
| 894 | 19785000 | ANT not only enhanced STZ-mediated insulin level decreases, but also decreased the triglyceride levels induced by STZ injection in serum. |
| 895 | 19785000 | Diabetic rats exhibited a lower expression of glucose transporter 4 proteins in the membrane fractions of heart and skeletal muscle tissues, which was enhanced by ANT. |
| 896 | 19785000 | In addition, ANT activated insulin receptor phosphorylation, suggesting an increased utilization of glucose by tissues. |
| 897 | 19785000 | Moreover, ANT protected pancreatic tissue from STZ-induced apoptosis through regulation of caspase-3, Bax, and Bcl-2 proteins. |
| 898 | 19785000 | Furthermore, ANT significantly suppressed malondialdehyde levels and restored superoxide dismutase and catalase activities in diabetic rats. |
| 899 | 19785000 | Taken together, ANT from black soybean seed coat have anti-diabetic effects that are due, in part, to the regulation of glucose transporter 4 and prevention of insulin resistance and pancreatic apoptosis, suggesting a possible use as a drug to regulate diabetes. |
| 900 | 19808082 | Angiotensin II-induced p53-dependent cardiac apoptotic cell death: its prevention by metallothionein. |
| 901 | 19808082 | The present study was to investigate whether Ang II induces p53 expression and activation and if so, whether Ang II-induced cardiac cell death is p53-dependent, and whether a potent antioxidant metallothionein (MT) prevents Ang II-induced p53 expression, and associate apoptotic cell death signaling. |
| 902 | 19808082 | We found that exposure of H9c2 cells to Ang II at 10, 50 and 100 nM for 24 h induced a significant apoptotic effect, measured by DNA fragmentation and cleaved caspase-3. |
| 903 | 19808082 | Induction of apoptotic cell death by Ang II can be completely blocked by p53 inhibitor Pitithrin-alpha. |
| 904 | 19808082 | Exposure of H9c2 cells to Ang II also significantly increased p53 phosphorylation, DNA double strand breaks and Bax/Bcl-2 ratio. |
| 905 | 19808082 | All these effects were not observed in H9c2MT7 cells that forcedly overexpresses human MT-IIA gene, suggesting the preventive effect of antioxidant MT against Ang II-induced p53 activation and its apoptotic death signaling. |
| 906 | 19808082 | Furthermore, the in vitro finding was validated in animal models by supplying Ang II to wild-type mice (WT) and MT-TG mice that has cardiac-specifically overexpressed MT gene. |
| 907 | 19808082 | Ang II-induced significant up-regulation of p53 expression along with an increase in Bax/Bcl-2 ratio in the hearts of WT mice, but not MT-TG mice. |
| 908 | 19808082 | These results suggest that Ang II-induced cardiac apoptotic cell death is mediated by p53 apoptotic signaling pathway, which is related to oxidative stress. |
| 909 | 19808082 | Antioxidant MT can completely prevent Ang II-induced p53 activation and associated apoptotic effect in the heart. |
| 910 | 19808082 | Angiotensin II-induced p53-dependent cardiac apoptotic cell death: its prevention by metallothionein. |
| 911 | 19808082 | The present study was to investigate whether Ang II induces p53 expression and activation and if so, whether Ang II-induced cardiac cell death is p53-dependent, and whether a potent antioxidant metallothionein (MT) prevents Ang II-induced p53 expression, and associate apoptotic cell death signaling. |
| 912 | 19808082 | We found that exposure of H9c2 cells to Ang II at 10, 50 and 100 nM for 24 h induced a significant apoptotic effect, measured by DNA fragmentation and cleaved caspase-3. |
| 913 | 19808082 | Induction of apoptotic cell death by Ang II can be completely blocked by p53 inhibitor Pitithrin-alpha. |
| 914 | 19808082 | Exposure of H9c2 cells to Ang II also significantly increased p53 phosphorylation, DNA double strand breaks and Bax/Bcl-2 ratio. |
| 915 | 19808082 | All these effects were not observed in H9c2MT7 cells that forcedly overexpresses human MT-IIA gene, suggesting the preventive effect of antioxidant MT against Ang II-induced p53 activation and its apoptotic death signaling. |
| 916 | 19808082 | Furthermore, the in vitro finding was validated in animal models by supplying Ang II to wild-type mice (WT) and MT-TG mice that has cardiac-specifically overexpressed MT gene. |
| 917 | 19808082 | Ang II-induced significant up-regulation of p53 expression along with an increase in Bax/Bcl-2 ratio in the hearts of WT mice, but not MT-TG mice. |
| 918 | 19808082 | These results suggest that Ang II-induced cardiac apoptotic cell death is mediated by p53 apoptotic signaling pathway, which is related to oxidative stress. |
| 919 | 19808082 | Antioxidant MT can completely prevent Ang II-induced p53 activation and associated apoptotic effect in the heart. |
| 920 | 19944681 | Myocardial infarct size, activities of ERK1/2, Bcl2, Bax and cytochrome c, and gene expression influencing Ca(2+) homeostasis were assessed. |
| 921 | 19944681 | Remifentanil preconditioning increased expression of ERK1/2 and anti-apoptotic protein Bcl-2 and decreased expression of pro-apoptotic proteins, Bax and cytochrome c, compared to ischemia-reperfusion only in wild-type rats. |
| 922 | 19944681 | Myocardial infarct size, activities of ERK1/2, Bcl2, Bax and cytochrome c, and gene expression influencing Ca(2+) homeostasis were assessed. |
| 923 | 19944681 | Remifentanil preconditioning increased expression of ERK1/2 and anti-apoptotic protein Bcl-2 and decreased expression of pro-apoptotic proteins, Bax and cytochrome c, compared to ischemia-reperfusion only in wild-type rats. |
| 924 | 19948220 | Decreases on Mn-superoxide dismutase (SOD), catalase, and heme oxygenase-1 levels by I/R were increased by sulforaphane treatment and pretreatment of 5-HD blocked the sulforaphane effects. |
| 925 | 19948220 | Increases in Bax and caspase-3 levels, and decrease in Bcl-2 level by I/R were attenuated by sulforaphane treatment. |
| 926 | 19966057 | Ten weeks following injection, diabetic hearts displayed increased caspase-3 and caspase-9 activities, indicating enhanced apoptotic signaling (P < 0.05, for both). |
| 927 | 19966057 | Furthermore, diabetic IFM possessed lower cytochrome c and BcL-2 levels and increased Bax levels (P < 0.05, for all 3). |
| 928 | 20127524 | PPAR-gamma, by increasing superoxide dismutase/catalase and decreasing nicotinamide adenine dinucleotide phosphate oxidase levels, attenuated ischemia-induced reactive oxygen species and subsequently alleviated the postischemic degradation of Bcl-2, Bcl-xl, and Akt. |
| 929 | 20200776 | Relationship between apoptotic markers (Bax and Bcl-2) and biochemical markers in type 2 diabetes mellitus. |
| 930 | 20363911 | Diabetes of 2 months duration caused a significant decrease in expression of Bcl-2 in retina, upregulation of Bax in whole retina and isolated retinal microvessels, and increased generation of retinal superoxide and leukostasis. |
| 931 | 20363911 | Furthermore, overexpression of Bcl-2 in the vascular endothelium inhibited the diabetes-induced degeneration of retinal capillaries and aberrant superoxide generation, but had no effect on Bax expression or leukostasis. |
| 932 | 20363911 | Diabetes of 2 months duration caused a significant decrease in expression of Bcl-2 in retina, upregulation of Bax in whole retina and isolated retinal microvessels, and increased generation of retinal superoxide and leukostasis. |
| 933 | 20363911 | Furthermore, overexpression of Bcl-2 in the vascular endothelium inhibited the diabetes-induced degeneration of retinal capillaries and aberrant superoxide generation, but had no effect on Bax expression or leukostasis. |
| 934 | 20374430 | To characterize the neuroprotective properties of GLP-1 and associated underlying mechanisms, we over-expressed the GLP-1 receptor (GLP-1R) on human neuroblastoma SH-SY5Y cells to generate a neuronal culture system featuring enhanced GLP-1R signaling. |
| 935 | 20374430 | In GLP-1R over-expressing SH-SY5Y (SH-hGLP-1R#9) cells, GLP-1 and the long-acting agonist exendin-4 stimulated cell proliferation and increased cell viability by 2-fold at 24 h at physiologically relevant concentrations. |
| 936 | 20374430 | This GLP-1R-dependent action was mediated via the protein kinase A and phosphoinositide 3-kinase signaling pathways, with the MAPK pathway playing a minor role. |
| 937 | 20374430 | This involved amelioration of elevated caspase 3 activity, down-regulation of pro-apoptotic Bax and up-regulation of anti-apoptotic Bcl-2 protein. |
| 938 | 20374430 | In the presence of 6-hydroxydopamine, GLP-1's ability to lower caspase-3 activity was abolished with the phosphoinositide 3-kinase inhibitor, LY2940002, and partly reduced with the protein kinase A inhibitor, H89. |
| 939 | 20374430 | Hence, GLP-1R mediated neurotrophic and anti-apoptotic actions co-contribute to the neuroprotective property of GLP-1 in neuronal cell cultures, and reinforce the potential therapeutic value of GLP-1R agonists in neurodegenerative disorders involving oxidative stress. |
| 940 | 20382773 | On day 70, plasma glucose levels, plasma and pancreatic insulin levels, pancreatic islet area and number, insulin and pancreatic/duodenal homeobox-1 (Pdx1) gene expression, and antiapoptotic BCL2 protein expression were determined. |
| 941 | 20382773 | Finally, in STZ-treated animals, UAG and Ob up-regulated insulin and Pdx1 mRNA and increased the expression of BCL2 similarly to AG. |
| 942 | 20382773 | On day 70, plasma glucose levels, plasma and pancreatic insulin levels, pancreatic islet area and number, insulin and pancreatic/duodenal homeobox-1 (Pdx1) gene expression, and antiapoptotic BCL2 protein expression were determined. |
| 943 | 20382773 | Finally, in STZ-treated animals, UAG and Ob up-regulated insulin and Pdx1 mRNA and increased the expression of BCL2 similarly to AG. |
| 944 | 20395372 | In addition, Bcl-2 transfection inhibited apoptosis and attenuated albumin-induced Bax translocation to mitochondria and cytochrome c release from the organelles, further confirming a role for the intrinsic pathway of apoptosis in albuminuria-associated tubular apoptosis. |
| 945 | 20395372 | Rottlerin, a pharmacologic inhibitor of PKC-delta, suppressed albumin-induced Bax translocation, cytochrome c release, and apoptosis. |
| 946 | 20506110 | PA-induced activation of CB(1)R is prevented by the treatment of AACOCF(3) (a cPLA(2) inhibitor), indomethacin and NS398 (a COX 2 inhibitors). |
| 947 | 20506110 | Indeed, PA increased cPLA(2), and COX-2 but not COX-1. |
| 948 | 20506110 | Furthermore, PA decreased GRP78 expression and induced increases in the endoplasmic reticulum (ER) stress signaling pathways p-PERK, p-eIF2α, p-ATF4, and CHOP, which were blocked by AM251 treatment. |
| 949 | 20506110 | Moreover, PA increased the Bax/Bcl-2 ratio, cleaved PARP, and caspase-3 levels. |
| 950 | 20532811 | Apoptotic factors (Bcl-2 and Bax) and diabetic retinopathy in type 2 diabetes. |
| 951 | 20532811 | The expression of apoptotic factors Bcl-2 and Bax were studied in the conjunctiva of diabetic patients with and without retinopathy. |
| 952 | 20532811 | In normal human conjunctiva, Bax showed positive expression in epithelial, vascular and stromal cells whereas Bcl-2 staining was negative. |
| 953 | 20532811 | Immunoreactivity was not correlated between Bcl-2 and Bax in the conjunctiva of diabetic patients. |
| 954 | 20532811 | Bax was always localized in tissues characterized by a high rate of apoptosis, whereas, Bcl-2 was absent. |
| 955 | 20532811 | Apoptotic factors (Bcl-2 and Bax) and diabetic retinopathy in type 2 diabetes. |
| 956 | 20532811 | The expression of apoptotic factors Bcl-2 and Bax were studied in the conjunctiva of diabetic patients with and without retinopathy. |
| 957 | 20532811 | In normal human conjunctiva, Bax showed positive expression in epithelial, vascular and stromal cells whereas Bcl-2 staining was negative. |
| 958 | 20532811 | Immunoreactivity was not correlated between Bcl-2 and Bax in the conjunctiva of diabetic patients. |
| 959 | 20532811 | Bax was always localized in tissues characterized by a high rate of apoptosis, whereas, Bcl-2 was absent. |
| 960 | 20532811 | Apoptotic factors (Bcl-2 and Bax) and diabetic retinopathy in type 2 diabetes. |
| 961 | 20532811 | The expression of apoptotic factors Bcl-2 and Bax were studied in the conjunctiva of diabetic patients with and without retinopathy. |
| 962 | 20532811 | In normal human conjunctiva, Bax showed positive expression in epithelial, vascular and stromal cells whereas Bcl-2 staining was negative. |
| 963 | 20532811 | Immunoreactivity was not correlated between Bcl-2 and Bax in the conjunctiva of diabetic patients. |
| 964 | 20532811 | Bax was always localized in tissues characterized by a high rate of apoptosis, whereas, Bcl-2 was absent. |
| 965 | 20532811 | Apoptotic factors (Bcl-2 and Bax) and diabetic retinopathy in type 2 diabetes. |
| 966 | 20532811 | The expression of apoptotic factors Bcl-2 and Bax were studied in the conjunctiva of diabetic patients with and without retinopathy. |
| 967 | 20532811 | In normal human conjunctiva, Bax showed positive expression in epithelial, vascular and stromal cells whereas Bcl-2 staining was negative. |
| 968 | 20532811 | Immunoreactivity was not correlated between Bcl-2 and Bax in the conjunctiva of diabetic patients. |
| 969 | 20532811 | Bax was always localized in tissues characterized by a high rate of apoptosis, whereas, Bcl-2 was absent. |
| 970 | 20532811 | Apoptotic factors (Bcl-2 and Bax) and diabetic retinopathy in type 2 diabetes. |
| 971 | 20532811 | The expression of apoptotic factors Bcl-2 and Bax were studied in the conjunctiva of diabetic patients with and without retinopathy. |
| 972 | 20532811 | In normal human conjunctiva, Bax showed positive expression in epithelial, vascular and stromal cells whereas Bcl-2 staining was negative. |
| 973 | 20532811 | Immunoreactivity was not correlated between Bcl-2 and Bax in the conjunctiva of diabetic patients. |
| 974 | 20532811 | Bax was always localized in tissues characterized by a high rate of apoptosis, whereas, Bcl-2 was absent. |
| 975 | 20542491 | Benfotiamine improves functional recovery of the infarcted heart via activation of pro-survival G6PD/Akt signaling pathway and modulation of neurohormonal response. |
| 976 | 20542491 | Furthermore, diabetic mice demonstrated increased cardiomyocyte apoptosis, reduced reparative angiogenesis, larger scars, enhanced oxidative stress, and blunted activation of the pro-survival VEGF receptor-2/Akt/Pim-1 signaling pathway. |
| 977 | 20542491 | In addition, BFT stimulated the activity of pentose phosphate pathway enzymes, leading to reduction of oxidative stress, phosphorylation/activation of VEGF receptor-2 and Akt and increased Pim-1, pBad and Bcl-2 levels. |
| 978 | 20542491 | These effects were contrasted on silencing glucose-6-phosphate dehydrogenase, the key enzyme in pentose phosphate pathway, or inhibiting Akt. |
| 979 | 20562294 | Methylglyoxal-induced imbalance in the ratio of vascular endothelial growth factor to angiopoietin 2 secreted by retinal pigment epithelial cells leads to endothelial dysfunction. |
| 980 | 20562294 | In this study, we hypothesize that increased levels of MGO disrupt the ratio of vascular endothelial growth factor (VEGF) to angiopoietin 2 (Ang 2) secreted by retinal pigment epithelial (RPE) cells, which provides a key destabilizing signal that leads to apoptosis and decreased proliferation of retinal endothelial cells. |
| 981 | 20562294 | Downregulation of VEGF is likely to be related to decreased hypoxia-inducible factor-1alpha (HIF-1alpha) protein levels and HIF-1 transcriptional activity. |
| 982 | 20562294 | Data further show that MGO-induced imbalance in the VEGF/Ang II ratio significantly changes the levels of BAX and Bcl-2 in endothelial cells. |
| 983 | 20562294 | Data obtained in cell culture systems are consistent with observations in retinas of diabetic animals, where increased availability of MGO is associated with changes in distribution and levels of HIF-1alpha, VEGF and Ang 2 and increased microvascular permeability. |
| 984 | 20562294 | In conclusion, the MGO-induced imbalance in the VEGF/Ang 2 ratio secreted by retinal epithelial cells activates apoptosis and decreases proliferation of retinal endothelial cells, which are likely to contribute to endothelial dysfunction in diabetic retinopathy. |
| 985 | 20574430 | After 12 weeks, Bax (apoptotic factor), Bcl(2) (B-cell lymphoma 2; anti-apoptotic factor), cGMP (cyclic guanosine monophosphate) were estimated in their cavernous tissues. |
| 986 | 20574430 | Compared with the controls, aged diabetic rats showed significant increased cavernous tissue Bax and significant decreased Bcl(2), in which diabetic rats injected with T showed the reverse compared with the diabetic rats. |
| 987 | 20574430 | Diabetic rats on sildenafil or tadalafil showed significant increased cavernous Bcl(2) and decreased Bax with upgraded Bcl(2)/Bax ratio that was improved being on T. |
| 988 | 20574430 | Diabetic rats on alternate sildenafil/tadalafil with or without T showed further significant increased cavernous tissue Bcl(2) with upgraded Bcl(2)/Bax ratio. |
| 989 | 20574430 | After 12 weeks, Bax (apoptotic factor), Bcl(2) (B-cell lymphoma 2; anti-apoptotic factor), cGMP (cyclic guanosine monophosphate) were estimated in their cavernous tissues. |
| 990 | 20574430 | Compared with the controls, aged diabetic rats showed significant increased cavernous tissue Bax and significant decreased Bcl(2), in which diabetic rats injected with T showed the reverse compared with the diabetic rats. |
| 991 | 20574430 | Diabetic rats on sildenafil or tadalafil showed significant increased cavernous Bcl(2) and decreased Bax with upgraded Bcl(2)/Bax ratio that was improved being on T. |
| 992 | 20574430 | Diabetic rats on alternate sildenafil/tadalafil with or without T showed further significant increased cavernous tissue Bcl(2) with upgraded Bcl(2)/Bax ratio. |
| 993 | 20574430 | After 12 weeks, Bax (apoptotic factor), Bcl(2) (B-cell lymphoma 2; anti-apoptotic factor), cGMP (cyclic guanosine monophosphate) were estimated in their cavernous tissues. |
| 994 | 20574430 | Compared with the controls, aged diabetic rats showed significant increased cavernous tissue Bax and significant decreased Bcl(2), in which diabetic rats injected with T showed the reverse compared with the diabetic rats. |
| 995 | 20574430 | Diabetic rats on sildenafil or tadalafil showed significant increased cavernous Bcl(2) and decreased Bax with upgraded Bcl(2)/Bax ratio that was improved being on T. |
| 996 | 20574430 | Diabetic rats on alternate sildenafil/tadalafil with or without T showed further significant increased cavernous tissue Bcl(2) with upgraded Bcl(2)/Bax ratio. |
| 997 | 20574430 | After 12 weeks, Bax (apoptotic factor), Bcl(2) (B-cell lymphoma 2; anti-apoptotic factor), cGMP (cyclic guanosine monophosphate) were estimated in their cavernous tissues. |
| 998 | 20574430 | Compared with the controls, aged diabetic rats showed significant increased cavernous tissue Bax and significant decreased Bcl(2), in which diabetic rats injected with T showed the reverse compared with the diabetic rats. |
| 999 | 20574430 | Diabetic rats on sildenafil or tadalafil showed significant increased cavernous Bcl(2) and decreased Bax with upgraded Bcl(2)/Bax ratio that was improved being on T. |
| 1000 | 20574430 | Diabetic rats on alternate sildenafil/tadalafil with or without T showed further significant increased cavernous tissue Bcl(2) with upgraded Bcl(2)/Bax ratio. |
| 1001 | 20610922 | Pathological examination revealed hypercellularity of spindle cells, that showed positive for CD34, vimentin, desmin and Mic-2, and negative for S100, alphaSMA, c-kit, AE1/3, p53 and bcl-2. |
| 1002 | 20654738 | Voltage-dependent anion channel (VDAC), adenine nucleotide translocator (ANT), cyclophilin D (CypD), transcription factor A (Tfam), Bax, Bcl-2 contents, caspase-3 and -9 activities were determined. |
| 1003 | 20654738 | Additionally, endurance training reverted the hyperglycemia-induced CypD elevation, attenuating decrease of ANT, VDAC and Tfam. |
| 1004 | 20654738 | Moreover, training prevented the STZ-induced elevation in Bax, Bax-to-Bcl-2 ratio, caspase-3 and -9 and the increased Bcl-2. |
| 1005 | 20654738 | Voltage-dependent anion channel (VDAC), adenine nucleotide translocator (ANT), cyclophilin D (CypD), transcription factor A (Tfam), Bax, Bcl-2 contents, caspase-3 and -9 activities were determined. |
| 1006 | 20654738 | Additionally, endurance training reverted the hyperglycemia-induced CypD elevation, attenuating decrease of ANT, VDAC and Tfam. |
| 1007 | 20654738 | Moreover, training prevented the STZ-induced elevation in Bax, Bax-to-Bcl-2 ratio, caspase-3 and -9 and the increased Bcl-2. |
| 1008 | 20660595 | Increased Bax/Bcl-2 expression ratio was observed in PMCA overexpressing β-cells. |
| 1009 | 20660595 | This was followed by Bax translocation to the mitochondria with subsequent cytochrome c release, opening of the permeability transition pore, and apoptosis. |
| 1010 | 20685070 | Erythropoietin (EPO) can induce a series of cytoprotective effects in many non-hematopoietic tissues through interaction with the erythropoietin receptor (EPOR), but whether EPO can prevent the overproduction of reactive oxygen species (ROS) and apoptosis in diabetes remains unclear. |
| 1011 | 20685070 | Here, we report that renal tubular cells possess EPOR and that EPO reduces high glucose-induced oxidative stress in renal tubular cells. |
| 1012 | 20685070 | Further, we found that EPO inhibited high glucose-induced renal tubular cell apoptosis and that this protective effect was dependent on reduction of Bax/caspase-3 expression as well as elevation of Bcl-2 expression. |
| 1013 | 20685070 | Our results suggest that EPO can inhibit high glucose-induced renal tubular cell apoptosis through direct effect on anti-oxidative stress and that EPOR may play a key role in this process. |
| 1014 | 20798690 | We presently evaluated the role of the myeloid cell leukemia sequence 1 (Mcl-1), an antiapoptotic protein of the Bcl-2 family, in β-cells following exposure to well-defined β-cell death effectors, for example, pro-inflammatory cytokines, palmitate and chemical endoplasmic reticulum (ER) stressors. |
| 1015 | 20798690 | All cytotoxic stresses rapidly and preferentially decreased Mcl-1 protein expression as compared with the late effect observed on the other antiapoptotic proteins, Bcl-2 and Bcl-xL. |
| 1016 | 20798690 | This was due to ER stress-mediated inhibition of translation through eIF2α phosphorylation for palmitate and ER stressors and through the combined action of translation inhibition and JNK activation for cytokines. |
| 1017 | 20798690 | Knocking down Mcl-1 using small interference RNAs increased apoptosis and caspase-3 cleavage induced by cytokines, palmitate or thapsigargin, whereas Mcl-1 overexpression partly prevented Bax translocation to the mitochondria, cytochrome c release, caspase-3 cleavage and apoptosis induced by the β-cell death effectors. |
| 1018 | 20798690 | We presently evaluated the role of the myeloid cell leukemia sequence 1 (Mcl-1), an antiapoptotic protein of the Bcl-2 family, in β-cells following exposure to well-defined β-cell death effectors, for example, pro-inflammatory cytokines, palmitate and chemical endoplasmic reticulum (ER) stressors. |
| 1019 | 20798690 | All cytotoxic stresses rapidly and preferentially decreased Mcl-1 protein expression as compared with the late effect observed on the other antiapoptotic proteins, Bcl-2 and Bcl-xL. |
| 1020 | 20798690 | This was due to ER stress-mediated inhibition of translation through eIF2α phosphorylation for palmitate and ER stressors and through the combined action of translation inhibition and JNK activation for cytokines. |
| 1021 | 20798690 | Knocking down Mcl-1 using small interference RNAs increased apoptosis and caspase-3 cleavage induced by cytokines, palmitate or thapsigargin, whereas Mcl-1 overexpression partly prevented Bax translocation to the mitochondria, cytochrome c release, caspase-3 cleavage and apoptosis induced by the β-cell death effectors. |
| 1022 | 20841353 | AMP-activated protein kinase mediates apoptosis in response to bioenergetic stress through activation of the pro-apoptotic Bcl-2 homology domain-3-only protein BMF. |
| 1023 | 20841353 | Interestingly, AMPK mediated the induction of the pro-apoptotic Bcl-2 homology domain-3-only protein Bmf (Bcl-2-modifying factor). |
| 1024 | 20841353 | This in turn mediates the transcriptional activation of the pro-apoptotic Bcl-2-homology protein BMF, coupling prolonged energy stress to apoptosis activation. |
| 1025 | 20841353 | AMP-activated protein kinase mediates apoptosis in response to bioenergetic stress through activation of the pro-apoptotic Bcl-2 homology domain-3-only protein BMF. |
| 1026 | 20841353 | Interestingly, AMPK mediated the induction of the pro-apoptotic Bcl-2 homology domain-3-only protein Bmf (Bcl-2-modifying factor). |
| 1027 | 20841353 | This in turn mediates the transcriptional activation of the pro-apoptotic Bcl-2-homology protein BMF, coupling prolonged energy stress to apoptosis activation. |
| 1028 | 20841353 | AMP-activated protein kinase mediates apoptosis in response to bioenergetic stress through activation of the pro-apoptotic Bcl-2 homology domain-3-only protein BMF. |
| 1029 | 20841353 | Interestingly, AMPK mediated the induction of the pro-apoptotic Bcl-2 homology domain-3-only protein Bmf (Bcl-2-modifying factor). |
| 1030 | 20841353 | This in turn mediates the transcriptional activation of the pro-apoptotic Bcl-2-homology protein BMF, coupling prolonged energy stress to apoptosis activation. |
| 1031 | 20933054 | This study demonstrates that pro-inflammatory cytokines strongly modified the expression of the anti-apoptotic protein Bcl-2 and the pro-apoptotic BH3-only proteins Bad, Bim, and Bid in primary rat islets and insulin-producing RINm5F cells. |
| 1032 | 20933054 | Overexpression of mitochondrially located catalase (MitoCatalase) specifically increased basal Bcl-2 and decreased basal Bax expression, suppressed cytokine-mediated reduction of Bcl-2, and thereby prevented the release of cytochrome c, Smac/DIABLO and the activation of caspase-9 and -3. |
| 1033 | 20933054 | Thus, cytokine-mediated decrease of Bcl-2 expression and the sequentially changed Bax/Bcl-2 ratio are responsible for the release of pro-apoptotic mitochondrial factors, activation of caspase-9, and ultimately caspase-3. |
| 1034 | 20933054 | These results indicate that activation of the intrinsic/mitochondrial apoptosis pathway is essential for cytokine-induced beta cell death and the mitochondrial generation of reactive oxygen species, in particular mitochondrial hydrogen peroxide, differentially regulates the Bax/Bcl-2 ratio. |
| 1035 | 20933054 | This study demonstrates that pro-inflammatory cytokines strongly modified the expression of the anti-apoptotic protein Bcl-2 and the pro-apoptotic BH3-only proteins Bad, Bim, and Bid in primary rat islets and insulin-producing RINm5F cells. |
| 1036 | 20933054 | Overexpression of mitochondrially located catalase (MitoCatalase) specifically increased basal Bcl-2 and decreased basal Bax expression, suppressed cytokine-mediated reduction of Bcl-2, and thereby prevented the release of cytochrome c, Smac/DIABLO and the activation of caspase-9 and -3. |
| 1037 | 20933054 | Thus, cytokine-mediated decrease of Bcl-2 expression and the sequentially changed Bax/Bcl-2 ratio are responsible for the release of pro-apoptotic mitochondrial factors, activation of caspase-9, and ultimately caspase-3. |
| 1038 | 20933054 | These results indicate that activation of the intrinsic/mitochondrial apoptosis pathway is essential for cytokine-induced beta cell death and the mitochondrial generation of reactive oxygen species, in particular mitochondrial hydrogen peroxide, differentially regulates the Bax/Bcl-2 ratio. |
| 1039 | 20933054 | This study demonstrates that pro-inflammatory cytokines strongly modified the expression of the anti-apoptotic protein Bcl-2 and the pro-apoptotic BH3-only proteins Bad, Bim, and Bid in primary rat islets and insulin-producing RINm5F cells. |
| 1040 | 20933054 | Overexpression of mitochondrially located catalase (MitoCatalase) specifically increased basal Bcl-2 and decreased basal Bax expression, suppressed cytokine-mediated reduction of Bcl-2, and thereby prevented the release of cytochrome c, Smac/DIABLO and the activation of caspase-9 and -3. |
| 1041 | 20933054 | Thus, cytokine-mediated decrease of Bcl-2 expression and the sequentially changed Bax/Bcl-2 ratio are responsible for the release of pro-apoptotic mitochondrial factors, activation of caspase-9, and ultimately caspase-3. |
| 1042 | 20933054 | These results indicate that activation of the intrinsic/mitochondrial apoptosis pathway is essential for cytokine-induced beta cell death and the mitochondrial generation of reactive oxygen species, in particular mitochondrial hydrogen peroxide, differentially regulates the Bax/Bcl-2 ratio. |
| 1043 | 20933054 | This study demonstrates that pro-inflammatory cytokines strongly modified the expression of the anti-apoptotic protein Bcl-2 and the pro-apoptotic BH3-only proteins Bad, Bim, and Bid in primary rat islets and insulin-producing RINm5F cells. |
| 1044 | 20933054 | Overexpression of mitochondrially located catalase (MitoCatalase) specifically increased basal Bcl-2 and decreased basal Bax expression, suppressed cytokine-mediated reduction of Bcl-2, and thereby prevented the release of cytochrome c, Smac/DIABLO and the activation of caspase-9 and -3. |
| 1045 | 20933054 | Thus, cytokine-mediated decrease of Bcl-2 expression and the sequentially changed Bax/Bcl-2 ratio are responsible for the release of pro-apoptotic mitochondrial factors, activation of caspase-9, and ultimately caspase-3. |
| 1046 | 20933054 | These results indicate that activation of the intrinsic/mitochondrial apoptosis pathway is essential for cytokine-induced beta cell death and the mitochondrial generation of reactive oxygen species, in particular mitochondrial hydrogen peroxide, differentially regulates the Bax/Bcl-2 ratio. |
| 1047 | 21078376 | Exacerbation of diabetes-induced testicular apoptosis by zinc deficiency is most likely associated with oxidative stress, p38 MAPK activation, and p53 activation in mice. |
| 1048 | 21078376 | TUNEL staining revealed that testicular apoptosis was significantly increased along with an increased Bax/Bcl-2 ratio, in diabetic mice and TPEN-treated normal mice. |
| 1049 | 21078376 | Increased oxidative stress was associated with an increase in activation of p38 MAPK and p53 protein in diabetic testis, which was worsened in the testes of diabetic mice with Zn deficiency. |
| 1050 | 21078376 | These results suggest that like diabetes, chronic depletion of Zn with TPEN induces testicular oxidative stress and damage, along with the activation of p38 MAPK and p53 signaling and mitochondria-related apoptotic cell death. |
| 1051 | 21139139 | A kinase-independent role for unoccupied insulin and IGF-1 receptors in the control of apoptosis. |
| 1052 | 21139139 | Insulin and insulin-like growth factor 1 (IGF-1) act as antiapoptotic hormones. |
| 1053 | 21139139 | We found that, unexpectedly, double-knockout (DKO) cells that lacked both insulin and IGF-1 receptors (IR and IGF1R, respectively) were resistant to apoptosis induced through either the intrinsic or the extrinsic pathway. |
| 1054 | 21139139 | This resistance to apoptosis was associated with decreased abundance of the proapoptotic protein Bax and increases in abundance of the antiapoptotic proteins Bcl-2, Bcl-xL, XIAP, and Flip. |
| 1055 | 21139139 | Insulin and IGF-1 binding stimulates receptor tyrosine kinase activity and blocks apoptosis, whereas unliganded IR and IGF1R, acting through a mechanism independent of their catalytic activity, exert a permissive effect on cell death. |
| 1056 | 21145380 | Here, we found that iAs significantly decreased insulin secretion and cell viability, and increased ROS and MDA formation in pancreatic β-cell-derived RIN-m5F cells. iAs also induced the increases in sub-G1 hypodiploids, annexin V-Cy3 binding, and caspase-3 activity in RIN-m5F cells, indicating that iAs could induce β-cell apoptosis. |
| 1057 | 21145380 | Moreover, iAs induced MAPKs activation, mitochondria dysfunction, p53 up-regulation, Bcl-2 and Mdm-2 down-regulation, PARP, and caspase cascades, which displayed features of mitochondria-dependent apoptotic signals. |
| 1058 | 21145380 | In addition, exposure of RIN-m5F cells to iAs, could trigger ER stress as indicated by the enhancement in ER stress-related molecules induction (such as GRP78, GRP94, CHOP, and XBP1), procaspase-12 cleavage, and calpain activation. |
| 1059 | 21151615 | Shen-Fu injection preconditioning inhibits myocardial ischemia-reperfusion injury in diabetic rats: activation of eNOS via the PI3K/Akt pathway. |
| 1060 | 21151615 | SFI preconditioning significantly decreased infarct size, apoptosis, caspase-3 protein expression, MDA level in myocardial tissues, and plasma level of CK and LDH but increased p-Akt, p-eNOS, bcl-2 protein expression, and SOD activity compared to I/R group. |
| 1061 | 21161439 | Cell viability, apoptosis, glucose-stimulated insulin secretion, Bcl-2, and Bax gene expression levels, mitochondrial membrane potential and cytochrome c release were examined. |
| 1062 | 21161439 | Linoleic acid also dose-dependently reduced mitochondrial membrane potential (ΔΨm) and significantly promoted cytochrome c release from mitochondria in both 11.1 mM glucose and 25 mM glucose culture medium, further reducing glucose-stimulated insulin secretion, which is dependent on normal mitochondrial function. |
| 1063 | 21163363 | Involvement of mitochondrial dysfunction in human islet amyloid polypeptide-induced apoptosis in INS-1E pancreatic beta cells: An effect attenuated by phycocyanin. |
| 1064 | 21163363 | Misfolded human islet amyloid polypeptide (hIAPP) in pancreatic islets is associated with the loss of insulin-secreting beta cells in type 2 diabetes. |
| 1065 | 21163363 | Further molecular analysis showed that hIAPP induced changes in the expression of Bcl-2 family members, release of cytochrome c and apoptosis-inducing factor (AIF) from mitochondria into cytosol, activation of caspases and cleavage of poly (ADP-ribose) polymerase. |
| 1066 | 21190961 | Here we investigated whether cytokine-induced inflammation and apoptosis can be prevented in β-cells by BCL-6 expression using plasmid, prolactin, and adenoviral approaches. |
| 1067 | 21190961 | The induction of mild or abundant BCL-6 expression in β-cells by prolactin or an adenoviral BCL-6 expression construct, respectively, reduced cytokine-induced inflammatory responses in a dose-dependent manner through inhibition of nuclear factor-κB activation. |
| 1068 | 21190961 | BCL-6 decreased Fas and inducible nitric oxide synthase expression and nitric oxide production, but it inhibited the expression of the antiapoptotic proteins Bcl-2 and JunB while increasing the expression of the proapoptotic death protein 5. |
| 1069 | 21273665 | Body weight and biochemical parameters (glucose, triglycerides, cholesterol), insulin and adipokines (leptin, adiponectin) were monitored. |
| 1070 | 21273665 | The microarray studies revealed that HF diet down-regulated genes related to angiogenesis (Nos3, Kdr) and up-regulated genes connected with apoptosis (activators of caspase 3, proapoptotic genes Bcl2) and proinflammatory pathway (NfκB pathway, Tnfα). |
| 1071 | 21289215 | The tuberin/mTOR pathway promotes apoptosis of tubular epithelial cells in diabetes. |
| 1072 | 21289215 | Because the tuberin/mTOR pathway can modulate apoptosis, we studied the role of this pathway in apoptosis in type I diabetes and in cultured proximal tubular epithelial (PTE) cells exposed to HG. |
| 1073 | 21289215 | Induction of diabetes also increased phosphorylation of tuberin in association with mTOR activation (measured by p70S6K phosphorylation), inactivation of Bcl-2, increased cytosolic cytochrome c expression, activation of caspase 3, and cleavage of PARP; insulin treatment prevented these changes. |
| 1074 | 21289215 | In vitro, exposure of PTE cells to HG increased phosphorylation of tuberin and p70S6K, phosphorylation of Bcl-2, expression of cytosolic cytochrome c, and caspase 3 activity. |
| 1075 | 21289215 | High glucose induced translocation of the caspase substrate YY1 from the cytoplasm to the nucleus and enhanced cleavage of PARP. |
| 1076 | 21289215 | Furthermore, gene silencing of tuberin with siRNA decreased cleavage of PARP. |
| 1077 | 21289215 | These data show that the tuberin/mTOR pathway promotes apoptosis of tubular epithelial cells in diabetes, mediated in part by cleavage of PARP by YY1. |
| 1078 | 21289215 | The tuberin/mTOR pathway promotes apoptosis of tubular epithelial cells in diabetes. |
| 1079 | 21289215 | Because the tuberin/mTOR pathway can modulate apoptosis, we studied the role of this pathway in apoptosis in type I diabetes and in cultured proximal tubular epithelial (PTE) cells exposed to HG. |
| 1080 | 21289215 | Induction of diabetes also increased phosphorylation of tuberin in association with mTOR activation (measured by p70S6K phosphorylation), inactivation of Bcl-2, increased cytosolic cytochrome c expression, activation of caspase 3, and cleavage of PARP; insulin treatment prevented these changes. |
| 1081 | 21289215 | In vitro, exposure of PTE cells to HG increased phosphorylation of tuberin and p70S6K, phosphorylation of Bcl-2, expression of cytosolic cytochrome c, and caspase 3 activity. |
| 1082 | 21289215 | High glucose induced translocation of the caspase substrate YY1 from the cytoplasm to the nucleus and enhanced cleavage of PARP. |
| 1083 | 21289215 | Furthermore, gene silencing of tuberin with siRNA decreased cleavage of PARP. |
| 1084 | 21289215 | These data show that the tuberin/mTOR pathway promotes apoptosis of tubular epithelial cells in diabetes, mediated in part by cleavage of PARP by YY1. |
| 1085 | 21296063 | Metoprolol inhibited CPT-1 without affecting CD36 translocation, associated with increased accumulation of triglycerides and long chain acyl CoA in the cytoplasm, and no effect on oxidative stress. |
| 1086 | 21296063 | Metoprolol induced a shift from protein kinase A to protein kinase B-mediated signaling, associated with a shift in the phosphorylation patterns of BCl-2 and Bad which favored BCl-2 action. |
| 1087 | 21312071 | In vitro, PTH1R silencing suppressed cell proliferation and apoptosis induced by high levels of glucose by regulating Bax/Bcl-2 expression. |
| 1088 | 21488836 | Among these factors, the cAMP-responsive element-binding protein (CREB) has emerged as a key transcriptional element for the maintenance of an efficient glucose sensing, insulin exocytosis, insulin gene transcription and β-cell survival. |
| 1089 | 21488836 | CREB activates the transcription of target genes within the β-cells in response to a diverse array of stimuli including glucose, incretin hormones such as the glucagon-like peptide-1 (GLP-1) or the gastric inhibitory polypeptide (GIP), the pituitary adenylate cyclase-activating polypeptide (PACAP), or growth factors such as the insulin like growth factor-1 (IGF-1). |
| 1090 | 21488836 | These mechanisms involve different protein kinases, scaffold proteins and cofactors which allow CREB to specifically regulate the expression of crucial genes such as insulin, BCL-2, cyclin D1, cyclin A2 or IRS-2. |
| 1091 | 21500593 | [Effects of nerve growth factor mixed insulin on angiogenesis of burn wounds and expressions of Bcl-2 and Bax in diabetic rats]. |
| 1092 | 21505475 | Cilostazol increased the number of B-cell lymphoma 2 (Bcl-2)-positive cells in both strains 48, 96, and 168 hours after 2VO, but did not improve vessel wall thickness or collagen deposits. |
| 1093 | 21505870 | Overexpression of lactadherin increased EC apoptosis with up-regulation of Bax/Bcl-2 ratio, cytochrome c release, caspase-9 and caspase-3 activation suggesting the involvement of mitochondria apoptosis pathway. |
| 1094 | 21590491 | Histology showed multiple rudimentary to well-formed, follicle-like cavities on a classical spindle cell background; while all the participating cells exhibited an SCO immunophenotype, including positivity for S100 protein, vimentin, EMA, Bcl-2, and TTF-1, as well as staining with the antimitochondrial antibody 113-1. |
| 1095 | 21625639 | Sphingosine kinase 1 regulates the Akt/FOXO3a/Bim pathway and contributes to apoptosis resistance in glioma cells. |
| 1096 | 21625639 | Further mechanistic study examined the expression of Bcl-2 family members, including Bcl-2, Mcl-1, Bax and Bim, in SPHK1-overexpressing glioma cells and revealed that only pro-apoptotic Bim was downregulated by SPHK1. |
| 1097 | 21625639 | Moreover, the transcriptional level of Bim was also altered by SPHK1 in glioma cells. |
| 1098 | 21625639 | We next confirmed the correlation between SPHK1 and Bim expression in primary glioma specimens. |
| 1099 | 21625639 | Importantly, increasing SPHK1 expression in glioma cells markedly elevated Akt activity and phosphorylated inactivation of FOXO3a, which led to downregulation of Bim. |
| 1100 | 21625639 | A pharmacological approach showed that these effects of SPHK1 were dependent on phosphatidylinositol 3-kinase (PI3K). |
| 1101 | 21625639 | Furthermore, effects of SPHK1 on Akt/FOXO3a/Bim pathway could be reversed by SPHK1 specific RNA interference or SPHK1 inhibitor. |
| 1102 | 21625639 | Collectively, our results indicate that regulation of the Akt/FOXO3a/Bim pathway may be a novel mechanism by which SPHK1 protects glioma cells from apoptosis, thereby involved in glioma tumorigenesis. |
| 1103 | 21667436 | Immunohistochemical and Western blot analyses revealed the downregulation of Bcl-2, upregulation of Bax, and increased activation of caspase-9 and -3, in diabetic rats, indicating that the apoptosis of taste bud cells may be mediated via the intrinsic mitochondrial pathway in diabetics. |
| 1104 | 21674480 | We used transgenic over-expression of either an anti-apoptotic protein (Bcl-2) or a toxic transgene (rat insulin promoter-Kb) in mouse β cells to reduce or increase neonatal β-cell apoptosis, respectively. |
| 1105 | 21742976 | Anti-CD3 treatment induced a transient systemic rise in the percentage but not absolute number of CD4(+)Foxp3(+) Tregs due to selective depletion of CD4(+)Foxp3(-) conventional T cells. |
| 1106 | 21742976 | T cell depletion induced by FNB anti-CD3 mAb was independent of the proapoptotic proteins Fas, caspase-3, and Bim and was not inhibited by overexpression of the anti-apoptotic protein, Bcl-2. |
| 1107 | 21773964 | The protein levels of p-AKT, Bcl-2, and Bax were also determined by Western blotting and immunohistochemistry, respectively. |
| 1108 | 21773964 | Furthermore, we found that glargine downregulated the level of Bax protein and upregulated that of Bcl-2 (p <0.05). |
| 1109 | 21773964 | The protein levels of p-AKT, Bcl-2, and Bax were also determined by Western blotting and immunohistochemistry, respectively. |
| 1110 | 21773964 | Furthermore, we found that glargine downregulated the level of Bax protein and upregulated that of Bcl-2 (p <0.05). |
| 1111 | 21776823 | Molecular and cellular studies indicated that metformin significantly elevated p53 and Bax levels and reduced STAT3 and Bcl-2. |
| 1112 | 21776823 | Receptor inhibitor studies indicated that p53 activation was mediated through insulin receptor (IR), not insulin-like growth factor-1 receptor (IGF-IR). |
| 1113 | 21776823 | Furthermore, MEK inhibitor significantly suppressed metformin-induced p53 and Bax elevation while ERK inhibitor generated a slight reduction in p53 levels. |
| 1114 | 21776823 | In contrast, PI3K inhibitor did not produce any effect on the metformin-elevated p53 levels. |
| 1115 | 21776823 | Finally, SAPK/JNK, known to be involved in apoptosis, was activated in cells treated with metformin and the activation appeared to occur downstream of ERK. |
| 1116 | 21776823 | All these results suggested that metformin activated p53, Bax, and induced tumor cell apoptosis through the ERK signaling pathway. |
| 1117 | 21776823 | This pathway has not been previously described for IR, p53, Bax activation, or apoptosis. |
| 1118 | 21805019 | The sensing of ribonucleic acids (RNAs) by the monocyte/macrophage system occurs through the TLR7/8 Toll-like receptor family, the retinoic acid-inducible protein I (RIG-I), and the melanoma differentiation-associated protein-5 (MDA-5). |
| 1119 | 21805019 | To determine whether circulating RNAs have an agonistic or antagonistic effect on the signaling pathways involved in inflammatory, apoptotic, and antiviral cascade, their effect on TLR8, RIG-I, MDA-5, MyD88, NF-KB, IRF-3, phosphoIRF-3, IRF-7, RIP, and p38 was evaluated. |
| 1120 | 21805019 | A significantly lower level was achieved by cultivating PBMCs with circulating RNAs isolated from type 1 diabetic children, compared to the intact PBMCs, in relation to TLR-8, MDA-5, NF-KB, phospho IRF-3, and RIP, while it was higher for Bax. |
| 1121 | 21805019 | All the metabolic stress conditions up-regulated NF-KB, Bcl-2, and Bax. |
| 1122 | 21839831 | We estimated blood glucose, glycosylated hemoglobin, glucokinase, and fructosamine and analyzed the expression of marker proteins like insulin, GLUT2, and GLUT4. |
| 1123 | 21839831 | We assayed generation of reactive oxygen species (ROS) and several inflammatory and apoptotic signal proteins like NFkB, IFNγ, iNOS, Bcl(2,) Bax, STAT1 and Caspase3. |
| 1124 | 21839831 | We observed an elevation of all biomarkers for oxidative stress, generation of ROS and activation of NFkB and down regulation in expression of insulin, GLUT2 and glucokinase in hyperglycemic mice. |
| 1125 | 21925162 | To examine the direct effects of EGCG on β-cells, insulin-producing RINm5F cells were exposed to a combination of recombinant interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), and interferon gamma (IFN-γ), with or without EGCG pretreatment for 24h. |
| 1126 | 21925162 | The expression of cytochrome c, Bax, Bcl-2, and iNOS proteins was measured by western blotting. |
| 1127 | 21925162 | EGCG reduced the cytokine-induced generation of reactive oxygen species, the loss of mitochondrial membrane potential (Δψm), the release of cytochrome c from the mitochondria, and translocation of Bax protein to the mitochondria from the cytosol. |
| 1128 | 21964948 | The relationship of CD4(+)CD25(hi) T regulatory cells (Treg) and pro-inflammatory Th17 and Th1 subsets in T2D patients with metabolic disorders and complications need to be determined. |
| 1129 | 21964948 | The ratios of CD4(+)CD25(hi) Treg/Th17 cells and CD4(+)CD25(hi) Treg/Th1 cells, but not Th17/Th1 cells, were significantly decreased in T2D patients. |
| 1130 | 21964948 | The thymic output CD4(+)Foxp3(+)Helios(+) Tregs were normal but peripheral induced CD4(+)Foxp3(+)Helios(-) Tregs were decreased in T2D patients. |
| 1131 | 21964948 | The Bcl-2/Bax ratio decreased in CD4(+)CD25(hi) Tregs in T2D patients, supporting the increased sensitivity to cell death of these cells in T2D. |
| 1132 | 21964948 | CD4(+)CD25(hi)CD127(-) Tregs in T2D patients with microvascular complications were significantly less than T2D patients with macrovascular complications. |
| 1133 | 21964948 | Importantly, CD4(+)CD25(hi)CD127(-) Tregs were positively correlated with plasma IL-6, whereas IL-17(+)CD4(+)cells were negatively related to high-density lipoprotein (HDL). |
| 1134 | 21977009 | Exposure to the viral by-product dsRNA or Coxsackievirus B5 triggers pancreatic beta cell apoptosis via a Bim / Mcl-1 imbalance. |
| 1135 | 21977009 | In this process, activation of the dsRNA-dependent protein kinase (PKR) promotes eIF2α phosphorylation and protein synthesis inhibition, leading to downregulation of the antiapoptotic Bcl-2 protein myeloid cell leukemia sequence 1 (Mcl-1). |
| 1136 | 21977009 | Mcl-1 decrease results in the release of the BH3-only protein Bim, which activates the mitochondrial pathway of apoptosis. |
| 1137 | 21977009 | Indeed, Bim knockdown prevented both dsRNA- and Coxsackievirus B5-induced beta cell death, and counteracted the proapoptotic effects of Mcl-1 silencing. |
| 1138 | 21977009 | These observations indicate that the balance between Mcl-1 and Bim is a key factor regulating beta cell survival during diabetogenic viral infections. |
| 1139 | 22037186 | This study examines the extent to which the antiapoptotic Bcl-2 proteins Bcl-2 and Bcl-x(L) contribute to diabetic Ca(2+) dysregulation and vessel contractility in vascular smooth muscle cells (VSMCs) through their interaction with inositol 1,4,5-trisphosphate receptor (InsP(3)R) intracellular Ca(2+) release channels. |
| 1140 | 22037186 | Protein expression levels of Bcl-x(L) but not Bcl-2 were elevated in VSMCs isolated from db/db compared with db/m age-matched controls. |
| 1141 | 22037186 | This study examines the extent to which the antiapoptotic Bcl-2 proteins Bcl-2 and Bcl-x(L) contribute to diabetic Ca(2+) dysregulation and vessel contractility in vascular smooth muscle cells (VSMCs) through their interaction with inositol 1,4,5-trisphosphate receptor (InsP(3)R) intracellular Ca(2+) release channels. |
| 1142 | 22037186 | Protein expression levels of Bcl-x(L) but not Bcl-2 were elevated in VSMCs isolated from db/db compared with db/m age-matched controls. |
| 1143 | 22138235 | Moreover, it increased oxidative stress (decreased antioxidant enzyme activities and GSH/GSSG ratio, increased xanthine oxidase enzyme activity, lipid peroxidation, protein carbonylation and ROS generation) and enhanced the proinflammatory cytokines levels, activity of myeloperoxidase and nuclear translocation of NFκB in the cardiac tissue of the experimental animals. |
| 1144 | 22138235 | In addition, taurine increased GLUT 4 translocation to the cardiac membrane by enhanced phosphorylation of IR and IRS1 at tyrosine and Akt at serine residue in the heart. |
| 1145 | 22138235 | Results also suggest that taurine could protect cardiac tissue from ALX induced apoptosis via the regulation of Bcl2 family and caspase 9/3 proteins. |
| 1146 | 22139526 | We examined the accumulation of argpyrimidine, a methylglyoxal-derived AGE, and the expression of apoptosis-related molecules including nuclear factor- kappaB (NF-κB), Bax, and Bcl-2 in the human LEC line HLE-B3 and in cataractous lenses of Zucker diabetic fatty (ZDF) rats, an animal model of type 2 diabetes. |
| 1147 | 22139526 | The ratio of Bax to Bcl-2 protein levels was also increased. |
| 1148 | 22139526 | We examined the accumulation of argpyrimidine, a methylglyoxal-derived AGE, and the expression of apoptosis-related molecules including nuclear factor- kappaB (NF-κB), Bax, and Bcl-2 in the human LEC line HLE-B3 and in cataractous lenses of Zucker diabetic fatty (ZDF) rats, an animal model of type 2 diabetes. |
| 1149 | 22139526 | The ratio of Bax to Bcl-2 protein levels was also increased. |
| 1150 | 22155658 | Further, western blot analysis revealed the activation of caspases family proteins viz., caspase 8, caspase-9 and caspase-3. |
| 1151 | 22155658 | An increase in the expression of Bax mRNA concomitant with a decrease in mRNA of Bcl-2 in BEHP treated K562 cells was also observed. |
| 1152 | 22179045 | We identified a putative BH3 (BCL2 homology 3) domain within this N-terminal CRK fragment, which sensitizes isolated mitochondria to cytochrome c release and when mutated significantly reduces the apoptotic activity of CRK in vivo. |
| 1153 | 22210314 | Bcl-2-modifying factor (Bmf) was differentially upregulated (P<0.01) in RPTs of db/db mice compared with db/m+ and db/db CAT-Tg mice and in RPTs of streptozotocin-induced diabetic mice in which insulin reversed this finding. |
| 1154 | 22210314 | In vitro, Bmf cDNA overexpression in rat RPTCs coimmunoprecipated with Bcl-2, enhanced caspase-3 activity, and promoted apoptosis. |
| 1155 | 22210314 | High glucose (25 mmol/L) induced Bmf mRNA expression in RPTCs, whereas rotenone, catalase, diphenylene iodinium, and apocynin decreased it. |
| 1156 | 22210314 | Bcl-2-modifying factor (Bmf) was differentially upregulated (P<0.01) in RPTs of db/db mice compared with db/m+ and db/db CAT-Tg mice and in RPTs of streptozotocin-induced diabetic mice in which insulin reversed this finding. |
| 1157 | 22210314 | In vitro, Bmf cDNA overexpression in rat RPTCs coimmunoprecipated with Bcl-2, enhanced caspase-3 activity, and promoted apoptosis. |
| 1158 | 22210314 | High glucose (25 mmol/L) induced Bmf mRNA expression in RPTCs, whereas rotenone, catalase, diphenylene iodinium, and apocynin decreased it. |
| 1159 | 22215602 | The proapoptotic Bcl-2 family member Bim is important for negative selection by inducing apoptosis in thymocytes receiving a strong signal through their antigen receptor. |
| 1160 | 22215602 | To study the role of Bim in clonal deletion to TRA, we constructed bone marrow (BM) chimeras using OT-I Bim-deficient or -sufficient donor bone marrow and recipients that express membrane bound chicken ovalbumin under control of the rat insulin promoter (Rip-mOVA). |
| 1161 | 22215602 | We found that clonal deletion to TRA was completely abrogated in the absence of Bim and large numbers of mature OT-I CD8 T cells survived in the periphery. |
| 1162 | 22220267 | Induction of protective genes in the recipient (e.g., heme oxygenase-1 (HO-1), A20/tumor necrosis factor alpha inducible protein3 (tnfaip3), biliverdin reductase (BVR), Bcl2, and others) or administration of one or more of the products of HO-1 to the donor, the islets themselves, and/or the recipient offers an alternative or synergistic approach to improve islet graft survival and function. |
| 1163 | 22220267 | In this perspective, we summarize studies describing the protective effects of these genes on islet survival and function in rodent allogeneic and xenogeneic transplantation models and the prevention of onset of diabetes, with emphasis on HO-1, A20, and BVR. |
| 1164 | 22235998 | Immunohistochemistry was used for identification of IL-17 and forkhead box protein 3 (FoxP3)-positive cells and quantitative polymerase chain reaction (qPCR) for IL-17, FoxP3, retinoic acid-related orphan receptor (ROR)c and interferon (IFN)-γ transcripts. |
| 1165 | 22235998 | IL-1β, IL-6 and IL-17 were studied in supernatants from biopsy cultures. |
| 1166 | 22235998 | Expression of the apoptotic markers BAX and bcl-2 was evaluated in IL-17-stimulated CaCo-2 cells. |
| 1167 | 22235998 | The mucosal expression of IL-17 and FoxP3 transcripts were elevated in individuals with untreated CD when compared with the TGA-negative reference children, children with potential CD or gluten-free diet-treated children with CD (P < 0·005 for all IL-17 comparisons and P < 0·01 for all FoxP3 comparisons). |
| 1168 | 22235998 | In biopsy specimens from patients with untreated CD, enhanced spontaneous secretion of IL-1β, IL-6 and IL-17 was seen. |
| 1169 | 22235998 | Activation of anti-apoptotic bcl-2 in IL-17-treated CaCo-2 epithelial cells suggests that IL-17 might be involved in mucosal protection. |
| 1170 | 22235998 | Immunohistochemistry was used for identification of IL-17 and forkhead box protein 3 (FoxP3)-positive cells and quantitative polymerase chain reaction (qPCR) for IL-17, FoxP3, retinoic acid-related orphan receptor (ROR)c and interferon (IFN)-γ transcripts. |
| 1171 | 22235998 | IL-1β, IL-6 and IL-17 were studied in supernatants from biopsy cultures. |
| 1172 | 22235998 | Expression of the apoptotic markers BAX and bcl-2 was evaluated in IL-17-stimulated CaCo-2 cells. |
| 1173 | 22235998 | The mucosal expression of IL-17 and FoxP3 transcripts were elevated in individuals with untreated CD when compared with the TGA-negative reference children, children with potential CD or gluten-free diet-treated children with CD (P < 0·005 for all IL-17 comparisons and P < 0·01 for all FoxP3 comparisons). |
| 1174 | 22235998 | In biopsy specimens from patients with untreated CD, enhanced spontaneous secretion of IL-1β, IL-6 and IL-17 was seen. |
| 1175 | 22235998 | Activation of anti-apoptotic bcl-2 in IL-17-treated CaCo-2 epithelial cells suggests that IL-17 might be involved in mucosal protection. |
| 1176 | 22249339 | Consequently, we evaluated the viability, the induction of apoptosis, the glucose-stimulated insulin secretion, and the expression of β-cell function genes (Isl1, Pax6, Glut-2, glucokinase) and apoptosis-related genes (Bax and Bcl2). βTC-1, βTC-6, and human islets treated, respectively, for 48 and 72 h with 15-30 nM MPA showed altered islet architecture, as compared with control cells. |
| 1177 | 22249339 | Furthermore, we showed significant down-regulation of gene expression of molecules involved in β-cell function and increase rate between Bax/Bcl2. |
| 1178 | 22249339 | Consequently, we evaluated the viability, the induction of apoptosis, the glucose-stimulated insulin secretion, and the expression of β-cell function genes (Isl1, Pax6, Glut-2, glucokinase) and apoptosis-related genes (Bax and Bcl2). βTC-1, βTC-6, and human islets treated, respectively, for 48 and 72 h with 15-30 nM MPA showed altered islet architecture, as compared with control cells. |
| 1179 | 22249339 | Furthermore, we showed significant down-regulation of gene expression of molecules involved in β-cell function and increase rate between Bax/Bcl2. |
| 1180 | 22266669 | Under the condition of hypoxia concomitant with serum deprivation, the overexpression of PGC-1α in MSCs resulted in a higher expression level of hypoxia-inducible factor-1α (Hif-1α), a greater ratio of B-cell lymphoma leukemia-2 (Bcl-2)/Bcl-2-associated X protein (Bax), and a lower level of caspase 3 compared with the controls, followed by an increased survival rate and an elevated expression level of several proangiogenic factors. |
| 1181 | 22302365 | In addition, hyperglycemia enhanced the levels of proinflammatory cytokins (TNF-α, IL-6, IL-1β) and Na(+)--K(+)-ATPase activity with a concomitant reduction in NO content and eNOS expression in diabetic kidney. |
| 1182 | 22302365 | However, taurine administration decreased the elevated blood glucose and proinflammatory cytokine levels, reduced renal oxidative stress (via decrease in xanthine oxidase activity, AGEs formation and inhibition of p47phox/CYP2E1 pathways), improved renal function and protected renal tissue from alloxan-induced apoptosis via the regulation of Bcl-2 family and caspase-9/3 proteins. |
| 1183 | 22341695 | Exercise training enhances cardiac IGFI-R/PI3K/Akt and Bcl-2 family associated pro-survival pathways in streptozotocin-induced diabetic rats. |
| 1184 | 22347430 | To this end, we presently evaluated the role of the transcription factor CCAAT/enhancer binding protein delta (C/EBPδ) on β-cell apoptosis and production of inflammatory mediators in the rat insulinoma INS-1E cells, in purified primary rat β-cells and in human islets. |
| 1185 | 22347430 | Small interfering RNA-mediated C/EBPδ silencing exacerbated IL-1β+IFN-γ-induced caspase 9 and 3 cleavage and apoptosis in these cells. |
| 1186 | 22347430 | C/EBPδ deficiency increased the up-regulation of the transcription factor CHOP in response to cytokines, enhancing expression of the pro-apoptotic Bcl-2 family member BIM. |
| 1187 | 22347430 | Interfering with C/EBPδ and CHOP or C/EBPδ and BIM in double knockdown approaches abrogated the exacerbating effects of C/EBPδ deficiency on cytokine-induced β-cell apoptosis, while C/EBPδ overexpression inhibited BIM expression and partially protected β-cells against IL-1β+IFN-γ-induced apoptosis. |
| 1188 | 22347430 | Furthermore, C/EBPδ silencing boosted cytokine-induced production of the chemokines CXCL1, 9, 10 and CCL20 in β-cells by hampering IRF-1 up-regulation and increasing STAT1 activation in response to cytokines. |
| 1189 | 22367460 | Bradykinin prevents the apoptosis of NIT-1 cells induced by TNF-α via the PI3K/Akt and MAPK signaling pathways. |
| 1190 | 22367460 | These effects were associated with upregulation of Bcl-2 and Bcl-xL protein expression levels as well as with downregulation of Bax expression levels via the activation of the mitogen-activated protein kinase and PI3K/Akt signaling pathways. |
| 1191 | 22391800 | Activated caspase 3 and Bax/Bcl-2 ratio-biochemical markers of apoptosis-were evaluated using immunoblotting. |
| 1192 | 22391800 | Administering SKE at a daily dose of between 50 and 200 mg/kg to the diabetic animals for 3 weeks ameliorated hyperglycemia, weight loss, hyperalgesia, and motor deficit, inhibited caspase 3 activation, and decreased the Bax/Bcl-2 ratio. |
| 1193 | 22391800 | Activated caspase 3 and Bax/Bcl-2 ratio-biochemical markers of apoptosis-were evaluated using immunoblotting. |
| 1194 | 22391800 | Administering SKE at a daily dose of between 50 and 200 mg/kg to the diabetic animals for 3 weeks ameliorated hyperglycemia, weight loss, hyperalgesia, and motor deficit, inhibited caspase 3 activation, and decreased the Bax/Bcl-2 ratio. |
| 1195 | 22447832 | Bax α protein expression was increased, while Bcl-2 was decreased. |
| 1196 | 22497970 | Simultaneously, resveratrol administration promoted the expression of SIRT1 in islets, while the expression of uncoupling protein 2 (UCP2) was restrained. |
| 1197 | 22497970 | Resveratrol, as well, also had a beneficial effect on the ratios of expressions of Bcl-2/Bax and levels of malondialdehyde/glutathione peroxidase. |
| 1198 | 22540890 | This tumor growth reduction was accompanied by the enhanced apoptotic cell death and an increase in Bax:Bcl2 ratio. |
| 1199 | 22540890 | The mechanism by which metformin manifests antitumor effects appears to be dependent on the inhibition of nuclear factor kappa B (NFkB) and mTOR signaling pathways. |
| 1200 | 22540890 | Decreased phosphorylation of NFkB inhibitory protein IKBα together with reduced enhancement of NFkB transcriptional target proteins, iNOS/COX-2 were observed. |
| 1201 | 22540890 | In addition, a decrease in the activation of ERK/p38-driven MAP kinase signaling was seen. |
| 1202 | 22540890 | Similarly, AKT signaling activation as assessed by the diminished phosphorylation at Ser473 with a concomitant decrease in mTOR signaling pathway was also noted as phosphorylation of mTOR regulatory proteins p70S6K and 4E-BP-1 was significantly reduced. |
| 1203 | 22540890 | These results suggest that metformin blocks SCC growth by dampening NFkB and mTOR signaling pathways. |
| 1204 | 22620683 | Further study demonstrated that LA upregulated Pdx1 and Bcl2 gene expression, reduced Bax gene expression, and promoted phosphorylation of Akt in HIT-T15 cells treated with high glucose. |
| 1205 | 22620683 | However, inhibition of Akt by PI3K/AKT antagonist LY294002 only slightly reversed the anti-apoptosis effect of LA and mildly decreased the gene expression level of Pdx1 (P > 0.05). |
| 1206 | 22644639 | Moreover, EHE treatment increased activities of antioxidant enzymes including catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-px) in high glucose pretreated INS-1 pancreatic β-cells. |
| 1207 | 22644639 | EHE slightly reduced the expression of pro-apoptotic protein Bax induced by high glucose but increased the expression of Bcl-2, an anti-apoptotic protein. |
| 1208 | 22653339 | We presently observed that CHOP knockdown (KD) prevents cytokine-mediated degradation of the anti-apoptotic proteins B-cell lymphoma 2 (Bcl-2) and myeloid cell leukemia sequence 1 (Mcl-1), thereby decreasing the cleavage of executioner caspases 9 and 3, and apoptosis. |
| 1209 | 22653339 | CHOP KD resulted in reduced cytokine-induced NF-κB activity and expression of key NF-κB target genes involved in apoptosis and inflammation, including iNOS, FAS, IRF-7, IL-15, CCL5 and CXCL10. |
| 1210 | 22718884 | Dipeptidyl peptidase 4 (DPP4) is an exopeptidase which modulates the function of its substrates, among which are insulin-releasing incretins. |
| 1211 | 22718884 | VG did not affect regeneration but decreased apoptosis, as shown by twofold decreased Bax/Bcl-2 mRNA expression and a threefold decrease in apoptotic bodies on terminal deoxynucleotidyl transferase dUTP nick-end labeling-stained sections. |
| 1212 | 22750288 | In the STZ group, TUNEL-staining levels and the expression of cleaved Caspase-3 and Bax were significantly increased, whereas Bcl-2 expression was significantly decreased. |
| 1213 | 22750288 | After the exposure to MG for 24h, cleaved Caspase-3 and Bax expression increased, whereas Bcl-2 expression decreased. |
| 1214 | 22750288 | These data suggest a possible link between the cognitive dysfunction associated with diabetes mellitus and the neurotoxicity of MG, which may alter the expression levels of cleaved Caspase-3, Bcl-2 and Bax in the hippocampus. |
| 1215 | 22750288 | In the STZ group, TUNEL-staining levels and the expression of cleaved Caspase-3 and Bax were significantly increased, whereas Bcl-2 expression was significantly decreased. |
| 1216 | 22750288 | After the exposure to MG for 24h, cleaved Caspase-3 and Bax expression increased, whereas Bcl-2 expression decreased. |
| 1217 | 22750288 | These data suggest a possible link between the cognitive dysfunction associated with diabetes mellitus and the neurotoxicity of MG, which may alter the expression levels of cleaved Caspase-3, Bcl-2 and Bax in the hippocampus. |
| 1218 | 22750288 | In the STZ group, TUNEL-staining levels and the expression of cleaved Caspase-3 and Bax were significantly increased, whereas Bcl-2 expression was significantly decreased. |
| 1219 | 22750288 | After the exposure to MG for 24h, cleaved Caspase-3 and Bax expression increased, whereas Bcl-2 expression decreased. |
| 1220 | 22750288 | These data suggest a possible link between the cognitive dysfunction associated with diabetes mellitus and the neurotoxicity of MG, which may alter the expression levels of cleaved Caspase-3, Bcl-2 and Bax in the hippocampus. |
| 1221 | 22774990 | The results indicated clearly that elevated MIF secretion preceded C57BL/6 pancreatic islets death induced by interferon (IFN)-γ + tumour necrosis factor (TNF)-α + interleukin (IL)-1β. |
| 1222 | 22774990 | Furthermore, upon exposure to cytokines pancreatic islets from MIF-KO mice maintained normal insulin expression and produced less cyclooxygenase-2 (COX-2) than those from wild-type C57BL6 mice. |
| 1223 | 22774990 | The final outcome of cytokine-induced islet apoptosis in islets from wild-type mice was the activation of mitochondrial membrane pore-forming protein Bcl-2-associated X protein and effector caspase 3. |
| 1224 | 22796564 | Furthermore, treatment with ALA down-regulated the Bax expression and the release of cytochrome c and AIF translocation, but up-regulated the Bcl-2 expression in SCs. |
| 1225 | 22796564 | Treatment with ALA attenuated the activation of caspase-3 and caspase-9 and minimized the cleavage of PARP in SCs. |
| 1226 | 22819546 | Small molecule kaempferol modulates PDX-1 protein expression and subsequently promotes pancreatic β-cell survival and function via CREB. |
| 1227 | 22819546 | In addition, kaempferol prevented the lipotoxicity-induced down-regulation of antiapoptotic proteins Akt and Bcl-2. |
| 1228 | 22819546 | The cytoprotective effects of kaempferol were associated with improved insulin secretion, synthesis, and pancreatic and duodenal homeobox-1 (PDX-1) expression. |
| 1229 | 22819546 | Chronic hyperlipidemia significantly diminished cyclic adenosine monophosphate (cAMP) production, protein kinase A (PKA) activation, cAMP-responsive element binding protein (CREB) phosphorylation and its regulated transcriptional activity in β-cells, all of which were restored by kaempferol treatment. |
| 1230 | 22819546 | PDX-1 gene knockdown reduced kaempferol-stimulated cAMP generation and CREB activation in INS-1E cells. |
| 1231 | 22819546 | These findings demonstrate that kaempferol is a novel survivor factor for pancreatic β-cells via up-regulating the PDX-1/cAMP/PKA/CREB signaling cascade. |
| 1232 | 22859217 | Furthermore, EPC transplantation decreased the expression of type I collagen, Bax, caspase-3 and p67phox, while increasing the expression of Bcl-2 and manganese superoxide dismutase (MnSOD). |
| 1233 | 22878185 | In addition, the dieckol treatment increased the activities of antioxidative enzymes including catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) in high glucose-pretreated rat insulinoma cells. |
| 1234 | 22878185 | These effects were mediated by suppressing apoptosis and were associated with increased anti-apoptotic Bcl-2 expression, and reduced pro-apoptotic cleaved caspase-3 expression. |
| 1235 | 22922276 | Exposure of pancreatic β-cells to cytokines, such as interleukin-1β (IL-1β), is thought to contribute to β-cell apoptosis. |
| 1236 | 22922276 | One important event triggered by IL-1β is induction of nitric oxide synthase (iNOS), an enzyme that catalyzes intracellular generation of the cytotoxic free radical NO. |
| 1237 | 22922276 | Our results demonstrate that formononetin significantly prevents IL-1β-increased INS-1 cell death and blocks cytokine-induced apoptotic signaling (the reduction of Bax/Bcl-2 ratio and caspase-3 activity). |
| 1238 | 22986487 | Body weight, food intake, lipid profiles, inflammatory markers (fibrinogen, Hs-CRP, IL-6, TNFα, and PAI-1), glycemic metabolism and insulin sensitivity, and apoptotic factors (Bcl-2 and Bax) expression were monitored. |
| 1239 | 22986487 | Moreover, liraglutide restored the islet structure, up-regulated Bcl-2 expression and down-regulated Bax expression. |
| 1240 | 22986487 | Body weight, food intake, lipid profiles, inflammatory markers (fibrinogen, Hs-CRP, IL-6, TNFα, and PAI-1), glycemic metabolism and insulin sensitivity, and apoptotic factors (Bcl-2 and Bax) expression were monitored. |
| 1241 | 22986487 | Moreover, liraglutide restored the islet structure, up-regulated Bcl-2 expression and down-regulated Bax expression. |
| 1242 | 23054864 | The results showed breast cancer cells respond in a diverse manner to LiCl, i.e., at lower concentrations (1, 5, and 10 mM), LiCl induces cell survival by inhibiting apoptosis through regulation of GSK-3β, caspase-2, Bax, and cleaved caspase-7 and by activating anti-apoptotic proteins (Akt, β-catenin, Bcl-2, and cyclin D1). |
| 1243 | 23138840 | In addition, ALX exposure reciprocally regulated Bcl-2 family protein expression, disturbed mitochondrial membrane potential, and subsequently released cytochrome c from mitochondria to cytosol. |
| 1244 | 23160962 | Further investigation found that upregulation of Bax and downregulation of Bcl2 was indeed induced by its expression, especially under high glucose conditions. |
| 1245 | 23193206 | Caspase induction and BCL2 inhibition in human adipose tissue: a potential relationship with insulin signaling alteration. |
| 1246 | 23222994 | Here, the different molecular mechanisms, effects, and pathophysiological implications of apoptosis and programmed necrosis are reviewed as they relate to heart failure and diabetes mediated by the Bcl-2 family protein, Nix. |
| 1247 | 23223177 | Dissociation of Bcl-2-Beclin1 complex by activated AMPK enhances cardiac autophagy and protects against cardiomyocyte apoptosis in diabetes. |
| 1248 | 23223177 | We hypothesized that AMPK-induced autophagy ameliorates diabetic cardiomyopathy by inhibiting cardiomyocyte apoptosis and examined the effects of AMPK on the interaction between Beclin1 and Bcl-2, a switch between autophagy and apoptosis, in diabetic mice and high glucose-treated H9c2 cardiac myoblast cells. |
| 1249 | 23223177 | Exposure of H9c2 cells to high glucose reduced AMPK activity, inhibited Jun NH2-terminal kinase 1 (JNK1)-B-cell lymphoma 2 (Bcl-2) signaling, and promoted Beclin1 binding to Bcl-2. |
| 1250 | 23223177 | Conversely, activation of AMPK by metformin stimulated JNK1-Bcl-2 signaling and disrupted the Beclin1-Bcl-2 complex. |
| 1251 | 23223177 | Finally, chronic administration of metformin in diabetic mice restored cardiac autophagy by activating JNK1-Bcl-2 pathways and dissociating Beclin1 and Bcl-2. |
| 1252 | 23223177 | We concluded that dissociation of Bcl-2 from Beclin1 may be an important mechanism for preventing diabetic cardiomyopathy via AMPK activation that restores autophagy and protects against cardiac apoptosis. |
| 1253 | 23223177 | Dissociation of Bcl-2-Beclin1 complex by activated AMPK enhances cardiac autophagy and protects against cardiomyocyte apoptosis in diabetes. |
| 1254 | 23223177 | We hypothesized that AMPK-induced autophagy ameliorates diabetic cardiomyopathy by inhibiting cardiomyocyte apoptosis and examined the effects of AMPK on the interaction between Beclin1 and Bcl-2, a switch between autophagy and apoptosis, in diabetic mice and high glucose-treated H9c2 cardiac myoblast cells. |
| 1255 | 23223177 | Exposure of H9c2 cells to high glucose reduced AMPK activity, inhibited Jun NH2-terminal kinase 1 (JNK1)-B-cell lymphoma 2 (Bcl-2) signaling, and promoted Beclin1 binding to Bcl-2. |
| 1256 | 23223177 | Conversely, activation of AMPK by metformin stimulated JNK1-Bcl-2 signaling and disrupted the Beclin1-Bcl-2 complex. |
| 1257 | 23223177 | Finally, chronic administration of metformin in diabetic mice restored cardiac autophagy by activating JNK1-Bcl-2 pathways and dissociating Beclin1 and Bcl-2. |
| 1258 | 23223177 | We concluded that dissociation of Bcl-2 from Beclin1 may be an important mechanism for preventing diabetic cardiomyopathy via AMPK activation that restores autophagy and protects against cardiac apoptosis. |
| 1259 | 23223177 | Dissociation of Bcl-2-Beclin1 complex by activated AMPK enhances cardiac autophagy and protects against cardiomyocyte apoptosis in diabetes. |
| 1260 | 23223177 | We hypothesized that AMPK-induced autophagy ameliorates diabetic cardiomyopathy by inhibiting cardiomyocyte apoptosis and examined the effects of AMPK on the interaction between Beclin1 and Bcl-2, a switch between autophagy and apoptosis, in diabetic mice and high glucose-treated H9c2 cardiac myoblast cells. |
| 1261 | 23223177 | Exposure of H9c2 cells to high glucose reduced AMPK activity, inhibited Jun NH2-terminal kinase 1 (JNK1)-B-cell lymphoma 2 (Bcl-2) signaling, and promoted Beclin1 binding to Bcl-2. |
| 1262 | 23223177 | Conversely, activation of AMPK by metformin stimulated JNK1-Bcl-2 signaling and disrupted the Beclin1-Bcl-2 complex. |
| 1263 | 23223177 | Finally, chronic administration of metformin in diabetic mice restored cardiac autophagy by activating JNK1-Bcl-2 pathways and dissociating Beclin1 and Bcl-2. |
| 1264 | 23223177 | We concluded that dissociation of Bcl-2 from Beclin1 may be an important mechanism for preventing diabetic cardiomyopathy via AMPK activation that restores autophagy and protects against cardiac apoptosis. |
| 1265 | 23223177 | Dissociation of Bcl-2-Beclin1 complex by activated AMPK enhances cardiac autophagy and protects against cardiomyocyte apoptosis in diabetes. |
| 1266 | 23223177 | We hypothesized that AMPK-induced autophagy ameliorates diabetic cardiomyopathy by inhibiting cardiomyocyte apoptosis and examined the effects of AMPK on the interaction between Beclin1 and Bcl-2, a switch between autophagy and apoptosis, in diabetic mice and high glucose-treated H9c2 cardiac myoblast cells. |
| 1267 | 23223177 | Exposure of H9c2 cells to high glucose reduced AMPK activity, inhibited Jun NH2-terminal kinase 1 (JNK1)-B-cell lymphoma 2 (Bcl-2) signaling, and promoted Beclin1 binding to Bcl-2. |
| 1268 | 23223177 | Conversely, activation of AMPK by metformin stimulated JNK1-Bcl-2 signaling and disrupted the Beclin1-Bcl-2 complex. |
| 1269 | 23223177 | Finally, chronic administration of metformin in diabetic mice restored cardiac autophagy by activating JNK1-Bcl-2 pathways and dissociating Beclin1 and Bcl-2. |
| 1270 | 23223177 | We concluded that dissociation of Bcl-2 from Beclin1 may be an important mechanism for preventing diabetic cardiomyopathy via AMPK activation that restores autophagy and protects against cardiac apoptosis. |
| 1271 | 23223177 | Dissociation of Bcl-2-Beclin1 complex by activated AMPK enhances cardiac autophagy and protects against cardiomyocyte apoptosis in diabetes. |
| 1272 | 23223177 | We hypothesized that AMPK-induced autophagy ameliorates diabetic cardiomyopathy by inhibiting cardiomyocyte apoptosis and examined the effects of AMPK on the interaction between Beclin1 and Bcl-2, a switch between autophagy and apoptosis, in diabetic mice and high glucose-treated H9c2 cardiac myoblast cells. |
| 1273 | 23223177 | Exposure of H9c2 cells to high glucose reduced AMPK activity, inhibited Jun NH2-terminal kinase 1 (JNK1)-B-cell lymphoma 2 (Bcl-2) signaling, and promoted Beclin1 binding to Bcl-2. |
| 1274 | 23223177 | Conversely, activation of AMPK by metformin stimulated JNK1-Bcl-2 signaling and disrupted the Beclin1-Bcl-2 complex. |
| 1275 | 23223177 | Finally, chronic administration of metformin in diabetic mice restored cardiac autophagy by activating JNK1-Bcl-2 pathways and dissociating Beclin1 and Bcl-2. |
| 1276 | 23223177 | We concluded that dissociation of Bcl-2 from Beclin1 may be an important mechanism for preventing diabetic cardiomyopathy via AMPK activation that restores autophagy and protects against cardiac apoptosis. |
| 1277 | 23223177 | Dissociation of Bcl-2-Beclin1 complex by activated AMPK enhances cardiac autophagy and protects against cardiomyocyte apoptosis in diabetes. |
| 1278 | 23223177 | We hypothesized that AMPK-induced autophagy ameliorates diabetic cardiomyopathy by inhibiting cardiomyocyte apoptosis and examined the effects of AMPK on the interaction between Beclin1 and Bcl-2, a switch between autophagy and apoptosis, in diabetic mice and high glucose-treated H9c2 cardiac myoblast cells. |
| 1279 | 23223177 | Exposure of H9c2 cells to high glucose reduced AMPK activity, inhibited Jun NH2-terminal kinase 1 (JNK1)-B-cell lymphoma 2 (Bcl-2) signaling, and promoted Beclin1 binding to Bcl-2. |
| 1280 | 23223177 | Conversely, activation of AMPK by metformin stimulated JNK1-Bcl-2 signaling and disrupted the Beclin1-Bcl-2 complex. |
| 1281 | 23223177 | Finally, chronic administration of metformin in diabetic mice restored cardiac autophagy by activating JNK1-Bcl-2 pathways and dissociating Beclin1 and Bcl-2. |
| 1282 | 23223177 | We concluded that dissociation of Bcl-2 from Beclin1 may be an important mechanism for preventing diabetic cardiomyopathy via AMPK activation that restores autophagy and protects against cardiac apoptosis. |
| 1283 | 23258905 | Dual Trade of Bcl-2 and Bcl-xL in islet physiology: balancing life and death with metabolism secretion coupling. |
| 1284 | 23267840 | All these events lead to excitotoxic neuronal death in the cerebral cortex, which was confirmed by the increased expression of caspase 3, caspase 8 and BCL2-associated X protein. |
| 1285 | 23304209 | Guizhi-Fuling-Wan, a Traditional Chinese Herbal Medicine, Ameliorates Memory Deficits and Neuronal Apoptosis in the Streptozotocin-Induced Hyperglycemic Rodents via the Decrease of Bax/Bcl2 Ratio and Caspase-3 Expression. |
| 1286 | 23304209 | It also was found that GFW treatment reduced caspase-3 protein levels and increased levels of the antiapoptotic protein Bcl-2 that were indicative of neuroprotection. |
| 1287 | 23304209 | Guizhi-Fuling-Wan, a Traditional Chinese Herbal Medicine, Ameliorates Memory Deficits and Neuronal Apoptosis in the Streptozotocin-Induced Hyperglycemic Rodents via the Decrease of Bax/Bcl2 Ratio and Caspase-3 Expression. |
| 1288 | 23304209 | It also was found that GFW treatment reduced caspase-3 protein levels and increased levels of the antiapoptotic protein Bcl-2 that were indicative of neuroprotection. |
| 1289 | 23328586 | The O-GlcNAc cycling mutants act, in part, by altering insulin signaling, proteasome activity and autophagy. |
| 1290 | 23328586 | In mutants lacking either of these enzymes of O-GlcNAc cycling, there is a striking accumulation of GFP::LGG-1 (C. elegans homolog of Atg8 and LC3) and increased phosphatidylethanolamine (PE)-modified GFP::LGG-1 upon starvation. |
| 1291 | 23328586 | We speculate that O-GlcNAc cycling is a key nutrient-responsive regulator of autophagic flux acting at multiple levels including direct modification of BECN1 and BCL2. |
| 1292 | 23380689 | We recently reported that diabetes depresses AMP-activated protein kinase (AMPK) activity, inhibits MAPK8/JNK1-BCL2 signaling, and promotes the interaction between BECN1 and BCL2. |
| 1293 | 23380689 | Activation of AMPK directly phosphorylates MAPK8, which mediates BCL2 phosphorylation and subsequent BECN1-BCL2 dissociation, leading to restoration of cardiac autophagy, protection against cardiac apoptosis, and ultimately improvement in cardiac structure and function. |
| 1294 | 23380689 | We conclude that dissociation of BCL2 from BECN1 through activation of MAPK8-BCL2 signaling may be an important mechanism by which AMPK activation restores autophagy, protects against cardiac apoptosis, and prevents diabetic cardiomyopathy. |
| 1295 | 23380689 | We recently reported that diabetes depresses AMP-activated protein kinase (AMPK) activity, inhibits MAPK8/JNK1-BCL2 signaling, and promotes the interaction between BECN1 and BCL2. |
| 1296 | 23380689 | Activation of AMPK directly phosphorylates MAPK8, which mediates BCL2 phosphorylation and subsequent BECN1-BCL2 dissociation, leading to restoration of cardiac autophagy, protection against cardiac apoptosis, and ultimately improvement in cardiac structure and function. |
| 1297 | 23380689 | We conclude that dissociation of BCL2 from BECN1 through activation of MAPK8-BCL2 signaling may be an important mechanism by which AMPK activation restores autophagy, protects against cardiac apoptosis, and prevents diabetic cardiomyopathy. |
| 1298 | 23380689 | We recently reported that diabetes depresses AMP-activated protein kinase (AMPK) activity, inhibits MAPK8/JNK1-BCL2 signaling, and promotes the interaction between BECN1 and BCL2. |
| 1299 | 23380689 | Activation of AMPK directly phosphorylates MAPK8, which mediates BCL2 phosphorylation and subsequent BECN1-BCL2 dissociation, leading to restoration of cardiac autophagy, protection against cardiac apoptosis, and ultimately improvement in cardiac structure and function. |
| 1300 | 23380689 | We conclude that dissociation of BCL2 from BECN1 through activation of MAPK8-BCL2 signaling may be an important mechanism by which AMPK activation restores autophagy, protects against cardiac apoptosis, and prevents diabetic cardiomyopathy. |
| 1301 | 23392943 | The results showed that STZ induced a significant increase in apoptotic rate of pancreatic islet cells, up-regulated the expression of bax and Fas and down-regulated the expression of Bcl-2, which were significantly blocked by taurine (P < 0.05). |
| 1302 | 23405080 | Cd also increased intracellular reactive oxygen species (ROS) generation and malondialdehyde (MDA) production and induced mitochondrial dysfunction (the loss of mitochondrial membrane potential (MMP) and the increase of cytosolic cytochrome c release), the decreased Bcl-2 expression, increased p53 expression, poly (ADP-ribose) polymerase (PARP) cleavage, and caspase cascades, which accompanied with intracellular Cd accumulation. |
| 1303 | 23405080 | Furthermore, exposure to Cd induced the phosphorylations of c-jun N-terminal kinases (JNK), extracellular signal-regulated kinases (ERK)1/2, and p38-mitogen-activated protein kinase (MAPK), which was prevented by NAC. |
| 1304 | 23405080 | Additionally, the specific JNK inhibitor SP600125 or JNK-specific small interference RNA (si-RNA) transfection suppressed Cd-induced β-cell apoptosis and related signals, but not ERK1/2 and p38-MAPK inhibitors (PD98059 and SB203580) did not. |
| 1305 | 23415873 | Stimulation of human T cells with PHA or CD3/CD28 induced IL-2 mRNA expression and activated the endoplasmic reticulum (ER) stress response. |
| 1306 | 23415873 | The treatment of T cells with curcumin induced the unfolded protein response (UPR) signaling pathway, initiated by the phosphorylation of PERK and IRE1. |
| 1307 | 23415873 | Furthermore, curcumin increased the expression of the ER stress associated transcriptional factors XBP-1, cleaved p50ATF6α and C/EBP homologous protein (CHOP) in human CD4+ and Jurkat T cells. |
| 1308 | 23415873 | In PHA-activated T cells, curcumin further enhanced PHA-induced CHOP expression and reduced the expression of the anti-apoptotic protein Bcl-2. |
| 1309 | 23427186 | The corpus cavernosum of untreated diabetic rats showed increased p47(phox) and p67(phox) expression, ROS production and penile apoptotic index, and decreased phospho-endothelial nitric oxide synthase (phospho-eNOS, Ser1177) expression, cGMP concentration, B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) ratio and smooth muscle cell number. |
| 1310 | 23427186 | SAC treatment normalized all the diabetes-induced effects, whereas insulin treatment partially normalized the alterations, but produced no effects on P47(phox) expression, penile ROS level, apoptotic index, Bcl-2/Bax ratio and smooth muscle cell number. |
| 1311 | 23427186 | The corpus cavernosum of untreated diabetic rats showed increased p47(phox) and p67(phox) expression, ROS production and penile apoptotic index, and decreased phospho-endothelial nitric oxide synthase (phospho-eNOS, Ser1177) expression, cGMP concentration, B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) ratio and smooth muscle cell number. |
| 1312 | 23427186 | SAC treatment normalized all the diabetes-induced effects, whereas insulin treatment partially normalized the alterations, but produced no effects on P47(phox) expression, penile ROS level, apoptotic index, Bcl-2/Bax ratio and smooth muscle cell number. |
| 1313 | 23440507 | Integrated analysis indicated that overexpression of PDP1, TRIB1, C13orf27, FOXA2, PMEPA1 and PHACTR3 was associated with gains, and underexpression of FHOD, SMAD4 and BCL2 was associated with losses. |
| 1314 | 23451817 | Real-time polymerase chain reaction and Western Blotting were performed to determine the expression of apoptosis-related genes and proteins such as Caspase-3, Bcl-2/Bax, Cyclin D1, and p21. |
| 1315 | 23499715 | Deletion of Fgf21 gene does not affect testicular cell proliferation, but significantly increases the spontaneous incidence of testicular TUNEL positive cells with increases in the Bax/Bcl2 expression ratio and apoptosis-inducing factor (AIF) expression. |
| 1316 | 23499715 | Diabetes induced significant increases in testicular TUNEL positive cells, Bax/Bcl2 expression ratio, AIF expression, CHOP and cleaved caspase-12 expression, and oxidative damage, but did not change the expression of cleaved caspase-3 and caspase-8. |
| 1317 | 23499715 | Deletion of Fgf21 gene also significantly enhances diabetes-induced TUNEL positive cells along with the increased expression of Bax/Bcl2 ratio, AIF, CHOP, cleaved caspase-12, and oxidative damage, which was significantly prevented by the supplementation of exogenous FGF21. |
| 1318 | 23499715 | Deletion of Fgf21 gene does not affect testicular cell proliferation, but significantly increases the spontaneous incidence of testicular TUNEL positive cells with increases in the Bax/Bcl2 expression ratio and apoptosis-inducing factor (AIF) expression. |
| 1319 | 23499715 | Diabetes induced significant increases in testicular TUNEL positive cells, Bax/Bcl2 expression ratio, AIF expression, CHOP and cleaved caspase-12 expression, and oxidative damage, but did not change the expression of cleaved caspase-3 and caspase-8. |
| 1320 | 23499715 | Deletion of Fgf21 gene also significantly enhances diabetes-induced TUNEL positive cells along with the increased expression of Bax/Bcl2 ratio, AIF, CHOP, cleaved caspase-12, and oxidative damage, which was significantly prevented by the supplementation of exogenous FGF21. |
| 1321 | 23499715 | Deletion of Fgf21 gene does not affect testicular cell proliferation, but significantly increases the spontaneous incidence of testicular TUNEL positive cells with increases in the Bax/Bcl2 expression ratio and apoptosis-inducing factor (AIF) expression. |
| 1322 | 23499715 | Diabetes induced significant increases in testicular TUNEL positive cells, Bax/Bcl2 expression ratio, AIF expression, CHOP and cleaved caspase-12 expression, and oxidative damage, but did not change the expression of cleaved caspase-3 and caspase-8. |
| 1323 | 23499715 | Deletion of Fgf21 gene also significantly enhances diabetes-induced TUNEL positive cells along with the increased expression of Bax/Bcl2 ratio, AIF, CHOP, cleaved caspase-12, and oxidative damage, which was significantly prevented by the supplementation of exogenous FGF21. |
| 1324 | 23500445 | In addition, PSG-1 inhibited the expression of pro-apoptotic protein, Bax and increased the expression of anti-apoptotic protein, Bcl-2 in pancreatic cells, suggesting that PSG-1 exerted a protective role in the pancreas of diabetic rats. |
| 1325 | 23521341 | A significant recovery was noted (P < 0.05) in the expression of Bax and Bcl-2 gene towards the control after the treatment of said fraction. |
| 1326 | 23525487 | We hypothesized that the abnormal FKBP12.6, SERCA2a, and CASQ2 are consequent to ER stress and apoptosis that are likely due to an entity of inflammation. |
| 1327 | 23525487 | FKBP12.6, SERCA2a, and CASQ2 and ER stress chaperones Bip and PERK and apoptotic molecules were monitored in vivo and in vitro. |
| 1328 | 23525487 | Impaired cardiac performance and downregulated FKBP12.6, SERCA2a, and CASQ2 were significant in DC in vivo, and abnormal calcium-handling proteins were also found in high-glucose-incubated myocytes in vitro. |
| 1329 | 23525487 | ER stress manifested by upregulated Bip and PERK was predominant in association with DNA ladder and upregulated Bax and downregulated BCL-2 in vivo and in vitro. |
| 1330 | 23533514 | Further confirmation of autophagy was obtained when western blots showed reduced Bcl-2 and increased Beclin-1, Atg 7 and 12 upon BMW treatment. |
| 1331 | 23533514 | The extracts also decreased the expression of DCLK1 and Lgr5, markers of quiescent, and activated stem cells. |
| 1332 | 23592481 | The sub-G0 cell population was higher with p21 overexpression and was attributable to apoptosis, as demonstrated by increased annexin-positive stained cells and cleaved caspase-3 protein. p21-mediated caspase-3 cleavage was inhibited by either overexpression of the antiapoptotic mitochondrial protein Bcl-2 or siRNA-mediated suppression of the proapoptotic proteins Bax and Bak. |
| 1333 | 23605050 | Effects of high iron and glucose concentrations over the relative expression of Bcl2, Bax, and Mfn2 in MIN6 cells. |
| 1334 | 23605050 | Hyperglycemia is linked to mitochondrial dysfunction and reduced β-cell mass due to the reduced expression of genes such as Mfn2 as well as the participation of the Bcl2 gene family, responsible for increased apoptosis. |
| 1335 | 23605050 | The purpose of this study was to describe the effect of different iron and/or glucose concentrations over Mfn2, Bax, and Bcl2 expressions in a β-pancreatic cell line (MIN6 cells). |
| 1336 | 23605050 | MIN6 cells were pre-incubated with different iron and/or glucose concentrations, and the relative mRNA abundance of the Bcl2/Bax ratio and of Mfn2 genes was measured by qRT-PCR. |
| 1337 | 23605050 | The Bcl2/Bax ratio increased and Mfn2 expression decreased in MIN6 cells after glucose stimulation. |
| 1338 | 23605050 | Our study revealed that high glucose/Fe concentrations in MIN6 cells induced an increase of the Bcl2/Bax ratio, an indicator of increased cell apoptosis. |
| 1339 | 23605050 | Effects of high iron and glucose concentrations over the relative expression of Bcl2, Bax, and Mfn2 in MIN6 cells. |
| 1340 | 23605050 | Hyperglycemia is linked to mitochondrial dysfunction and reduced β-cell mass due to the reduced expression of genes such as Mfn2 as well as the participation of the Bcl2 gene family, responsible for increased apoptosis. |
| 1341 | 23605050 | The purpose of this study was to describe the effect of different iron and/or glucose concentrations over Mfn2, Bax, and Bcl2 expressions in a β-pancreatic cell line (MIN6 cells). |
| 1342 | 23605050 | MIN6 cells were pre-incubated with different iron and/or glucose concentrations, and the relative mRNA abundance of the Bcl2/Bax ratio and of Mfn2 genes was measured by qRT-PCR. |
| 1343 | 23605050 | The Bcl2/Bax ratio increased and Mfn2 expression decreased in MIN6 cells after glucose stimulation. |
| 1344 | 23605050 | Our study revealed that high glucose/Fe concentrations in MIN6 cells induced an increase of the Bcl2/Bax ratio, an indicator of increased cell apoptosis. |
| 1345 | 23605050 | Effects of high iron and glucose concentrations over the relative expression of Bcl2, Bax, and Mfn2 in MIN6 cells. |
| 1346 | 23605050 | Hyperglycemia is linked to mitochondrial dysfunction and reduced β-cell mass due to the reduced expression of genes such as Mfn2 as well as the participation of the Bcl2 gene family, responsible for increased apoptosis. |
| 1347 | 23605050 | The purpose of this study was to describe the effect of different iron and/or glucose concentrations over Mfn2, Bax, and Bcl2 expressions in a β-pancreatic cell line (MIN6 cells). |
| 1348 | 23605050 | MIN6 cells were pre-incubated with different iron and/or glucose concentrations, and the relative mRNA abundance of the Bcl2/Bax ratio and of Mfn2 genes was measured by qRT-PCR. |
| 1349 | 23605050 | The Bcl2/Bax ratio increased and Mfn2 expression decreased in MIN6 cells after glucose stimulation. |
| 1350 | 23605050 | Our study revealed that high glucose/Fe concentrations in MIN6 cells induced an increase of the Bcl2/Bax ratio, an indicator of increased cell apoptosis. |
| 1351 | 23605050 | Effects of high iron and glucose concentrations over the relative expression of Bcl2, Bax, and Mfn2 in MIN6 cells. |
| 1352 | 23605050 | Hyperglycemia is linked to mitochondrial dysfunction and reduced β-cell mass due to the reduced expression of genes such as Mfn2 as well as the participation of the Bcl2 gene family, responsible for increased apoptosis. |
| 1353 | 23605050 | The purpose of this study was to describe the effect of different iron and/or glucose concentrations over Mfn2, Bax, and Bcl2 expressions in a β-pancreatic cell line (MIN6 cells). |
| 1354 | 23605050 | MIN6 cells were pre-incubated with different iron and/or glucose concentrations, and the relative mRNA abundance of the Bcl2/Bax ratio and of Mfn2 genes was measured by qRT-PCR. |
| 1355 | 23605050 | The Bcl2/Bax ratio increased and Mfn2 expression decreased in MIN6 cells after glucose stimulation. |
| 1356 | 23605050 | Our study revealed that high glucose/Fe concentrations in MIN6 cells induced an increase of the Bcl2/Bax ratio, an indicator of increased cell apoptosis. |
| 1357 | 23605050 | Effects of high iron and glucose concentrations over the relative expression of Bcl2, Bax, and Mfn2 in MIN6 cells. |
| 1358 | 23605050 | Hyperglycemia is linked to mitochondrial dysfunction and reduced β-cell mass due to the reduced expression of genes such as Mfn2 as well as the participation of the Bcl2 gene family, responsible for increased apoptosis. |
| 1359 | 23605050 | The purpose of this study was to describe the effect of different iron and/or glucose concentrations over Mfn2, Bax, and Bcl2 expressions in a β-pancreatic cell line (MIN6 cells). |
| 1360 | 23605050 | MIN6 cells were pre-incubated with different iron and/or glucose concentrations, and the relative mRNA abundance of the Bcl2/Bax ratio and of Mfn2 genes was measured by qRT-PCR. |
| 1361 | 23605050 | The Bcl2/Bax ratio increased and Mfn2 expression decreased in MIN6 cells after glucose stimulation. |
| 1362 | 23605050 | Our study revealed that high glucose/Fe concentrations in MIN6 cells induced an increase of the Bcl2/Bax ratio, an indicator of increased cell apoptosis. |
| 1363 | 23605050 | Effects of high iron and glucose concentrations over the relative expression of Bcl2, Bax, and Mfn2 in MIN6 cells. |
| 1364 | 23605050 | Hyperglycemia is linked to mitochondrial dysfunction and reduced β-cell mass due to the reduced expression of genes such as Mfn2 as well as the participation of the Bcl2 gene family, responsible for increased apoptosis. |
| 1365 | 23605050 | The purpose of this study was to describe the effect of different iron and/or glucose concentrations over Mfn2, Bax, and Bcl2 expressions in a β-pancreatic cell line (MIN6 cells). |
| 1366 | 23605050 | MIN6 cells were pre-incubated with different iron and/or glucose concentrations, and the relative mRNA abundance of the Bcl2/Bax ratio and of Mfn2 genes was measured by qRT-PCR. |
| 1367 | 23605050 | The Bcl2/Bax ratio increased and Mfn2 expression decreased in MIN6 cells after glucose stimulation. |
| 1368 | 23605050 | Our study revealed that high glucose/Fe concentrations in MIN6 cells induced an increase of the Bcl2/Bax ratio, an indicator of increased cell apoptosis. |
| 1369 | 23638232 | Immunohistochemically, the lymphoid cells were positive for vimentin, CD3, CD4, CD5, CD8, CD10, CD15, CD20, CD23, CD30, CD43, CD38, CD138, CD45RO, CD79α, bcl-2, bcl-6, κ-chain, λ-chain, and Ki-67 (labeling index=7%). |
| 1370 | 23638232 | The lymphoblastic cells were positively labeled for CD15 and CD30. |
| 1371 | 23638232 | They were negative for cytokeratin (CK) CAM5.2, CKAE1/3, CK34BE12, CK5/6, CK7, CK8, CK18, CK19, CK20, EMA, CEA, CD56, CD57, p53, KIT, PDGFRA, and cyclin D1. |
| 1372 | 23638232 | The low Ki-67 labeling and negative p53 also suggested the diagnosis. |
| 1373 | 23657598 | High glucose induces mitochondrial p53 phosphorylation by p38 MAPK in pancreatic RINm5F cells. |
| 1374 | 23657598 | This increased phosphorylation correlated with an increase in reactive oxygen species, a decrease in the Bcl-2/Bax ratio, a release of cytochrome c and an increase in the rate of apoptosis. |
| 1375 | 23657598 | To identify the kinase responsible for phosphorylating p53, p38 mitogen-activated protein kinase (MAPK) activation was analysed. |
| 1376 | 23657598 | We found that high glucose induced an increase in p38 MAPK phosphorylation in the mitochondria after 24-72 h. |
| 1377 | 23657598 | Moreover, the phosphorylation of p53 (ser392) by p38 MAPK in mitochondria was confirmed by colocalisation studies with confocal microscopy. |
| 1378 | 23657598 | The addition of a specific p38 MAPK inhibitor (SB203580) to the culture medium during high glucose treatment blocked p53 mobilisation to the mitochondria and phosphorylation; thus, the release of cytochrome c and the apoptosis rate in RINm5F cells decreased. |
| 1379 | 23657598 | These results suggest that mitochondrial p53 phosphorylation by p38 MAPK plays an important role in RINm5F cell death under high glucose conditions. |
| 1380 | 23671887 | MG caused a decrease of Bcl-2/Bax ratio (marker of apoptosis) and vWF staining (microvascular marker), what was partially reverted by the treatment with pyridoxamine. |
| 1381 | 23682852 | Compared with normal rats, the content of smooth muscle and B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) ratio were dramatically decreased, and penile apoptotic index and expression of activated-caspase-3 were dramatically increased in diabetic rats. |
| 1382 | 23717386 | Nutrient-deprivation autophagy factor-1 (NAF-1) (synonyms: Cisd2, Eris, Miner1, and Noxp70) is a [2Fe-2S] cluster protein immune-detected both in endoplasmic reticulum (ER) and mitochondrial outer membrane. |
| 1383 | 23717386 | It was implicated in human pathology (Wolfram Syndrome 2) and in BCL-2 mediated antagonization of Beclin 1-dependent autophagy and depression of ER calcium stores. |
| 1384 | 23745582 | The expression and distribution of claudin-5, occludin, acrolein, 8-OHdG and nitrotyrosine in the rat retinas were detected by immunofluorescent staining. |
| 1385 | 23745582 | The protein level of VEGFR2, Trx-2, Bcl-2, Bax, caspase-3, p53, and NF-κB in the rat retinas were assayed by western blot. |
| 1386 | 23745582 | Four months after subcutaneous injection, the diabetic rats treated with SS31 had better structures of retinal ganglion cells, thinner capillary basement membrane, less iBRB leakage, more uniform staining of claudin-5 and occludin in the retinal vessels, lower levels of acrolein, 8-OHdG, nitrotyrosine, Bax, caspase-3, p53, and NF-κB, and higher levels of Trx-2 and Bcl-2 in the retinas than those treated with N.S. |
| 1387 | 23745582 | In conclusion, SS31 could protect the retinal structures and inhibit the breakdown of iBRB by reducing oxidative damage, increasing Trx-2 and Bcl-2 expression, and decreasing p53, NF-κB, Bax, caspase-3, and VEGFR2 expression in the retinas of diabetic rats. |
| 1388 | 23745582 | The expression and distribution of claudin-5, occludin, acrolein, 8-OHdG and nitrotyrosine in the rat retinas were detected by immunofluorescent staining. |
| 1389 | 23745582 | The protein level of VEGFR2, Trx-2, Bcl-2, Bax, caspase-3, p53, and NF-κB in the rat retinas were assayed by western blot. |
| 1390 | 23745582 | Four months after subcutaneous injection, the diabetic rats treated with SS31 had better structures of retinal ganglion cells, thinner capillary basement membrane, less iBRB leakage, more uniform staining of claudin-5 and occludin in the retinal vessels, lower levels of acrolein, 8-OHdG, nitrotyrosine, Bax, caspase-3, p53, and NF-κB, and higher levels of Trx-2 and Bcl-2 in the retinas than those treated with N.S. |
| 1391 | 23745582 | In conclusion, SS31 could protect the retinal structures and inhibit the breakdown of iBRB by reducing oxidative damage, increasing Trx-2 and Bcl-2 expression, and decreasing p53, NF-κB, Bax, caspase-3, and VEGFR2 expression in the retinas of diabetic rats. |
| 1392 | 23745582 | The expression and distribution of claudin-5, occludin, acrolein, 8-OHdG and nitrotyrosine in the rat retinas were detected by immunofluorescent staining. |
| 1393 | 23745582 | The protein level of VEGFR2, Trx-2, Bcl-2, Bax, caspase-3, p53, and NF-κB in the rat retinas were assayed by western blot. |
| 1394 | 23745582 | Four months after subcutaneous injection, the diabetic rats treated with SS31 had better structures of retinal ganglion cells, thinner capillary basement membrane, less iBRB leakage, more uniform staining of claudin-5 and occludin in the retinal vessels, lower levels of acrolein, 8-OHdG, nitrotyrosine, Bax, caspase-3, p53, and NF-κB, and higher levels of Trx-2 and Bcl-2 in the retinas than those treated with N.S. |
| 1395 | 23745582 | In conclusion, SS31 could protect the retinal structures and inhibit the breakdown of iBRB by reducing oxidative damage, increasing Trx-2 and Bcl-2 expression, and decreasing p53, NF-κB, Bax, caspase-3, and VEGFR2 expression in the retinas of diabetic rats. |
| 1396 | 23778688 | Ventricular hemodynamic parameters were recorded; fasting blood glucose (FBG) and glycosylated hemoglobin (HbA1c) levels were determined using an automatic biochemistry analyzer; plasma interleukin (IL)-1, IL-4 and cardiac 4-hydroxynon-2-enal (4-HNE) levels were determined using enzyme-linked immunosorbent assay (ELISA), and cardiac ALDH2 activity was measured. |
| 1397 | 23778688 | The mRNA expression levels of Bax and Bcl-2 of the left anterior myocardium were detected by reverse transcriptase‑polymerase chain reaction (RT-PCR). |
| 1398 | 23778688 | The left ventricular developed pressure (LVDP), heart rate (HR) and rate-pressure product (RPP) were decreased, plasma IL-1 levels were increased, while IL-4 levels were decreased in the DM groups compared to the control group. |
| 1399 | 23778688 | Bax mRNA levels were increased, Bcl-2 mRNA levels were decreased, and Bcl-2/Bax mRNA ratios were decreased in the DM groups compared to the control group. |
| 1400 | 23778688 | Moreover, LVDP, HR, RPP, IL-4, ALDH2 activity and Bcl-2/Bax mRNA ratios were further reduced, while 4-HNE and IL-1 levels were increased with the progression of diabetes. |
| 1401 | 23778688 | Ventricular hemodynamic parameters were recorded; fasting blood glucose (FBG) and glycosylated hemoglobin (HbA1c) levels were determined using an automatic biochemistry analyzer; plasma interleukin (IL)-1, IL-4 and cardiac 4-hydroxynon-2-enal (4-HNE) levels were determined using enzyme-linked immunosorbent assay (ELISA), and cardiac ALDH2 activity was measured. |
| 1402 | 23778688 | The mRNA expression levels of Bax and Bcl-2 of the left anterior myocardium were detected by reverse transcriptase‑polymerase chain reaction (RT-PCR). |
| 1403 | 23778688 | The left ventricular developed pressure (LVDP), heart rate (HR) and rate-pressure product (RPP) were decreased, plasma IL-1 levels were increased, while IL-4 levels were decreased in the DM groups compared to the control group. |
| 1404 | 23778688 | Bax mRNA levels were increased, Bcl-2 mRNA levels were decreased, and Bcl-2/Bax mRNA ratios were decreased in the DM groups compared to the control group. |
| 1405 | 23778688 | Moreover, LVDP, HR, RPP, IL-4, ALDH2 activity and Bcl-2/Bax mRNA ratios were further reduced, while 4-HNE and IL-1 levels were increased with the progression of diabetes. |
| 1406 | 23778688 | Ventricular hemodynamic parameters were recorded; fasting blood glucose (FBG) and glycosylated hemoglobin (HbA1c) levels were determined using an automatic biochemistry analyzer; plasma interleukin (IL)-1, IL-4 and cardiac 4-hydroxynon-2-enal (4-HNE) levels were determined using enzyme-linked immunosorbent assay (ELISA), and cardiac ALDH2 activity was measured. |
| 1407 | 23778688 | The mRNA expression levels of Bax and Bcl-2 of the left anterior myocardium were detected by reverse transcriptase‑polymerase chain reaction (RT-PCR). |
| 1408 | 23778688 | The left ventricular developed pressure (LVDP), heart rate (HR) and rate-pressure product (RPP) were decreased, plasma IL-1 levels were increased, while IL-4 levels were decreased in the DM groups compared to the control group. |
| 1409 | 23778688 | Bax mRNA levels were increased, Bcl-2 mRNA levels were decreased, and Bcl-2/Bax mRNA ratios were decreased in the DM groups compared to the control group. |
| 1410 | 23778688 | Moreover, LVDP, HR, RPP, IL-4, ALDH2 activity and Bcl-2/Bax mRNA ratios were further reduced, while 4-HNE and IL-1 levels were increased with the progression of diabetes. |
| 1411 | 23797737 | Further studies found that pre-incubation with calycosin at 1 × 10(-8) M dramatically increased anti-apoptotic Bcl-2 while decreased pro-apoptotic Bax and Bad expressions as detected by immunocytochemistry, and the effect of calycosin on rebalancing the ratio of Bcl-2/Bax was more significant than that of its glycoside, calycosin-7-O-β-D-glucopyranoside (CG). |
| 1412 | 23808158 | The expression of the Bcl-2 family, c-fos, c-myc and p53 was measured by real-time PCR. |
| 1413 | 23808158 | EGCG decreased the Bcl-2/Bax expression stimulated by a high glucose. |
| 1414 | 23808158 | Moreover, EGCG suppressed the high glucose-induced expression of c-fos, c-myc and p53. |
| 1415 | 23808158 | These findings suggest that EGCG protects HLEB-3 cells from high glucose-induced apoptosis by regulating the gene expression of the Bcl-2 family, c-fos, c-myc and p53. |
| 1416 | 23808158 | The expression of the Bcl-2 family, c-fos, c-myc and p53 was measured by real-time PCR. |
| 1417 | 23808158 | EGCG decreased the Bcl-2/Bax expression stimulated by a high glucose. |
| 1418 | 23808158 | Moreover, EGCG suppressed the high glucose-induced expression of c-fos, c-myc and p53. |
| 1419 | 23808158 | These findings suggest that EGCG protects HLEB-3 cells from high glucose-induced apoptosis by regulating the gene expression of the Bcl-2 family, c-fos, c-myc and p53. |
| 1420 | 23808158 | The expression of the Bcl-2 family, c-fos, c-myc and p53 was measured by real-time PCR. |
| 1421 | 23808158 | EGCG decreased the Bcl-2/Bax expression stimulated by a high glucose. |
| 1422 | 23808158 | Moreover, EGCG suppressed the high glucose-induced expression of c-fos, c-myc and p53. |
| 1423 | 23808158 | These findings suggest that EGCG protects HLEB-3 cells from high glucose-induced apoptosis by regulating the gene expression of the Bcl-2 family, c-fos, c-myc and p53. |
| 1424 | 23811558 | Ginsenoside Rh1 significantly inhibited LPS/CHX-induced Akt phosphorylation, as well as mammalian target of rapamycin and Bcl-2-associated death promoter activation in both cell types. |
| 1425 | 23811558 | Furthermore, ginsenoside Rh1 inhibited pyruvate dehydrogenase lipoamide kinase isozyme 1 (PDK-1) phosphorylation. |
| 1426 | 23811558 | On the basis of these findings, we propose that ginsenoside Rh1 could possibly eliminate HIV-1 infected macrophages by inhibiting the PDK1/Akt pathway. |
| 1427 | 23884888 | β-cell-specific IL-2 therapy increases islet Foxp3+Treg and suppresses type 1 diabetes in NOD mice. |
| 1428 | 23884888 | Interleukin-2 (IL-2) is a critical cytokine for the homeostasis and function of forkhead box p3-expressing regulatory T cells (Foxp3(+)Tregs). |
| 1429 | 23884888 | Dysregulation of the IL-2-IL-2 receptor axis is associated with aberrant Foxp3(+)Tregs and T cell-mediated autoimmune diseases such as type 1 diabetes. |
| 1430 | 23884888 | Treatment with recombinant IL-2 has been reported to enhance Foxp3(+)Tregs and suppress different models of autoimmunity. |
| 1431 | 23884888 | However, efficacy of IL-2 therapy is dependent on achieving sufficient levels of IL-2 to boost tissue-resident Foxp3(+)Tregs while avoiding the potential toxic effects of systemic IL-2. |
| 1432 | 23884888 | Injection of a double-stranded AAV vector encoding IL-2 driven by a mouse insulin promoter (dsAAVmIP-IL2) increased Foxp3(+)Tregs in the islets but not the draining pancreatic lymph nodes. |
| 1433 | 23884888 | Islet Foxp3(+)Tregs in dsAAVmIP-IL2-treated NOD mice exhibited enhanced fitness marked by increased expression of Bcl-2, proliferation, and suppressor function. |
| 1434 | 23884888 | Collectively, these findings demonstrate that β-cell-specific IL-2 expands an islet-resident Foxp3(+)Tregs pool that effectively suppresses ongoing type 1 diabetes long term. |
| 1435 | 23923076 | Pancreases were double immuno-labeled to assess the islet morphology, insulin expression, expression of proliferation gene PCNA and anti-apoptosis gene bcl-2. |
| 1436 | 23927369 | The viability of mouse SVZ-derived NSCs and the involvement of apoptosis (Bcl-2, cleaved caspase-3) and unfolded protein response [C/EBP homologous protein (CHOP) Glucose-regulated protein 78/immunoglobulin heavy-chain binding protein (GRP78/BiP), spliced X-box binding protein 1 (XBP1), c-Jun N-terminal kinases (JNK) phosphorylation] were assessed in the presence of glucolipotoxic conditions after 24 h. |
| 1437 | 23954465 | We have previously reported that BBR attenuated H2O2 neurotoxicity via activating the PI3K/Akt/Nrf2-dependent pathway. |
| 1438 | 23954465 | However, AG1024, an inhibitor of insulin growth factor-1 (IGF-1) receptor, significantly abolished BBR protection against high glucose-induced neuronal death. |
| 1439 | 23954465 | BBR also increased Bcl-2 expression and decreased cytochrome c release. |
| 1440 | 23954465 | High glucose down-regulated IGF-1 receptor and phosphorylation of Akt and GSK-3β, the effects of which were attenuated by BBR treatment. |
| 1441 | 23954465 | BBR also activated nuclear erythroid 2-related factor 2 (Nrf2), the key antioxidative transcription factor, which is accompanied with up-regulation of hemeoxygenase-1 (HO-1). |
| 1442 | 23954465 | Results indicated Nrf2 siRNA abolished BBR-induced HO-1, NGF, neurite outgrowth and ROS decrease. |
| 1443 | 23985558 | Exposure to 25 mM glucose significantly reduced insulin content (p<0.05) and glucokinase activity (p<0.01) after 72 h. |
| 1444 | 23985558 | Effects of hyperglycemia on secretory function were accompanied by decreased mRNA expression of INS, GCK, PCSK1, PCSK2, PPP3CB, GJA1, ABCC8, and KCNJ11. |
| 1445 | 23985558 | Hyperglycemia-induced apoptosis was evident from increased activity of caspase 3/7 and decreased BCL2 protein. |
| 1446 | 24008114 | Expression of basic fibroblast growth factor, protein kinase C and members of the apoptotic pathway in skeletal muscle of streptozotocin-induced diabetic rats. |
| 1447 | 24008114 | Protein and mRNA levels of basic FGF (bFGF), bax, bcl-2, and caspase 3 in skeletal muscle were compared between the 2 groups using immunohistochemistry and quantitative PCR, respectively. |
| 1448 | 24008114 | Serum level of insulin and protein kinase C (PKC) were measured by competitive RIA and ELISA, respectively. |
| 1449 | 24008114 | Protein and mRNA levels of the apoptosis promoting genes caspase-3 and bax were higher in skeletal muscle from STZ-induced diabetic rats as compared to control animals (P<0.001 and P=0.037, respectively), while mRNA and protein levels of bcl-2, an inhibitor of apoptosis, was lower in STZ-induced diabetic rats versus control animals (P=0.026). |
| 1450 | 24008114 | Expression of basic fibroblast growth factor, protein kinase C and members of the apoptotic pathway in skeletal muscle of streptozotocin-induced diabetic rats. |
| 1451 | 24008114 | Protein and mRNA levels of basic FGF (bFGF), bax, bcl-2, and caspase 3 in skeletal muscle were compared between the 2 groups using immunohistochemistry and quantitative PCR, respectively. |
| 1452 | 24008114 | Serum level of insulin and protein kinase C (PKC) were measured by competitive RIA and ELISA, respectively. |
| 1453 | 24008114 | Protein and mRNA levels of the apoptosis promoting genes caspase-3 and bax were higher in skeletal muscle from STZ-induced diabetic rats as compared to control animals (P<0.001 and P=0.037, respectively), while mRNA and protein levels of bcl-2, an inhibitor of apoptosis, was lower in STZ-induced diabetic rats versus control animals (P=0.026). |
| 1454 | 18991018 | The timing of re-institution of good blood glucose control affects apoptosis and expression of Bax and Bcl-2 in the retina of diabetic rats. |
| 1455 | 18991018 | We explored the effect of re-institution of good blood glucose control on apoptosis and apoptosis related genes (Bax and Bcl-2) in the retina of diabetic rats. |
| 1456 | 18991018 | Expression of Bax and Bcl-2 in the retina was studied by immunohistochemistry and the apoptotic cells were stained using the TUNEL method. |
| 1457 | 18991018 | The apoptotic cell, expression of Bax and Bcl-2 and the ratio of Bax to Bcl-2 in the retina was increased in DM group compared with normal rats' (P < 0.01). |
| 1458 | 18991018 | There was no significant difference in apoptotic cells and the ratio of Bax to Bcl-2 between DM(1) group and CON group. |
| 1459 | 18991018 | The number of TUNEL positive cells and Bax to Bcl-2 ratio was partially reversed in DM(2) group. |
| 1460 | 18991018 | But glucose control had no effect on the apoptotic cells and the expression of Bax and Bcl-2 in DM(3) group. |
| 1461 | 18991018 | There was a positive correlation between apoptotic cells and Bax/Bcl-2 ratio in the retina (r = 0.808, P < 0.01). |
| 1462 | 18991018 | Good blood glucose control at early stage can decrease the number of apoptotic cells in the retina; the decreased apoptosis is correlated with the down-regulation of Bax to Bcl-2 ratio. |
| 1463 | 18991018 | The timing of re-institution of good blood glucose control affects apoptosis and expression of Bax and Bcl-2 in the retina of diabetic rats. |
| 1464 | 18991018 | We explored the effect of re-institution of good blood glucose control on apoptosis and apoptosis related genes (Bax and Bcl-2) in the retina of diabetic rats. |
| 1465 | 18991018 | Expression of Bax and Bcl-2 in the retina was studied by immunohistochemistry and the apoptotic cells were stained using the TUNEL method. |
| 1466 | 18991018 | The apoptotic cell, expression of Bax and Bcl-2 and the ratio of Bax to Bcl-2 in the retina was increased in DM group compared with normal rats' (P < 0.01). |
| 1467 | 18991018 | There was no significant difference in apoptotic cells and the ratio of Bax to Bcl-2 between DM(1) group and CON group. |
| 1468 | 18991018 | The number of TUNEL positive cells and Bax to Bcl-2 ratio was partially reversed in DM(2) group. |
| 1469 | 18991018 | But glucose control had no effect on the apoptotic cells and the expression of Bax and Bcl-2 in DM(3) group. |
| 1470 | 18991018 | There was a positive correlation between apoptotic cells and Bax/Bcl-2 ratio in the retina (r = 0.808, P < 0.01). |
| 1471 | 18991018 | Good blood glucose control at early stage can decrease the number of apoptotic cells in the retina; the decreased apoptosis is correlated with the down-regulation of Bax to Bcl-2 ratio. |
| 1472 | 18991018 | The timing of re-institution of good blood glucose control affects apoptosis and expression of Bax and Bcl-2 in the retina of diabetic rats. |
| 1473 | 18991018 | We explored the effect of re-institution of good blood glucose control on apoptosis and apoptosis related genes (Bax and Bcl-2) in the retina of diabetic rats. |
| 1474 | 18991018 | Expression of Bax and Bcl-2 in the retina was studied by immunohistochemistry and the apoptotic cells were stained using the TUNEL method. |
| 1475 | 18991018 | The apoptotic cell, expression of Bax and Bcl-2 and the ratio of Bax to Bcl-2 in the retina was increased in DM group compared with normal rats' (P < 0.01). |
| 1476 | 18991018 | There was no significant difference in apoptotic cells and the ratio of Bax to Bcl-2 between DM(1) group and CON group. |
| 1477 | 18991018 | The number of TUNEL positive cells and Bax to Bcl-2 ratio was partially reversed in DM(2) group. |
| 1478 | 18991018 | But glucose control had no effect on the apoptotic cells and the expression of Bax and Bcl-2 in DM(3) group. |
| 1479 | 18991018 | There was a positive correlation between apoptotic cells and Bax/Bcl-2 ratio in the retina (r = 0.808, P < 0.01). |
| 1480 | 18991018 | Good blood glucose control at early stage can decrease the number of apoptotic cells in the retina; the decreased apoptosis is correlated with the down-regulation of Bax to Bcl-2 ratio. |
| 1481 | 18991018 | The timing of re-institution of good blood glucose control affects apoptosis and expression of Bax and Bcl-2 in the retina of diabetic rats. |
| 1482 | 18991018 | We explored the effect of re-institution of good blood glucose control on apoptosis and apoptosis related genes (Bax and Bcl-2) in the retina of diabetic rats. |
| 1483 | 18991018 | Expression of Bax and Bcl-2 in the retina was studied by immunohistochemistry and the apoptotic cells were stained using the TUNEL method. |
| 1484 | 18991018 | The apoptotic cell, expression of Bax and Bcl-2 and the ratio of Bax to Bcl-2 in the retina was increased in DM group compared with normal rats' (P < 0.01). |
| 1485 | 18991018 | There was no significant difference in apoptotic cells and the ratio of Bax to Bcl-2 between DM(1) group and CON group. |
| 1486 | 18991018 | The number of TUNEL positive cells and Bax to Bcl-2 ratio was partially reversed in DM(2) group. |
| 1487 | 18991018 | But glucose control had no effect on the apoptotic cells and the expression of Bax and Bcl-2 in DM(3) group. |
| 1488 | 18991018 | There was a positive correlation between apoptotic cells and Bax/Bcl-2 ratio in the retina (r = 0.808, P < 0.01). |
| 1489 | 18991018 | Good blood glucose control at early stage can decrease the number of apoptotic cells in the retina; the decreased apoptosis is correlated with the down-regulation of Bax to Bcl-2 ratio. |
| 1490 | 18991018 | The timing of re-institution of good blood glucose control affects apoptosis and expression of Bax and Bcl-2 in the retina of diabetic rats. |
| 1491 | 18991018 | We explored the effect of re-institution of good blood glucose control on apoptosis and apoptosis related genes (Bax and Bcl-2) in the retina of diabetic rats. |
| 1492 | 18991018 | Expression of Bax and Bcl-2 in the retina was studied by immunohistochemistry and the apoptotic cells were stained using the TUNEL method. |
| 1493 | 18991018 | The apoptotic cell, expression of Bax and Bcl-2 and the ratio of Bax to Bcl-2 in the retina was increased in DM group compared with normal rats' (P < 0.01). |
| 1494 | 18991018 | There was no significant difference in apoptotic cells and the ratio of Bax to Bcl-2 between DM(1) group and CON group. |
| 1495 | 18991018 | The number of TUNEL positive cells and Bax to Bcl-2 ratio was partially reversed in DM(2) group. |
| 1496 | 18991018 | But glucose control had no effect on the apoptotic cells and the expression of Bax and Bcl-2 in DM(3) group. |
| 1497 | 18991018 | There was a positive correlation between apoptotic cells and Bax/Bcl-2 ratio in the retina (r = 0.808, P < 0.01). |
| 1498 | 18991018 | Good blood glucose control at early stage can decrease the number of apoptotic cells in the retina; the decreased apoptosis is correlated with the down-regulation of Bax to Bcl-2 ratio. |
| 1499 | 18991018 | The timing of re-institution of good blood glucose control affects apoptosis and expression of Bax and Bcl-2 in the retina of diabetic rats. |
| 1500 | 18991018 | We explored the effect of re-institution of good blood glucose control on apoptosis and apoptosis related genes (Bax and Bcl-2) in the retina of diabetic rats. |
| 1501 | 18991018 | Expression of Bax and Bcl-2 in the retina was studied by immunohistochemistry and the apoptotic cells were stained using the TUNEL method. |
| 1502 | 18991018 | The apoptotic cell, expression of Bax and Bcl-2 and the ratio of Bax to Bcl-2 in the retina was increased in DM group compared with normal rats' (P < 0.01). |
| 1503 | 18991018 | There was no significant difference in apoptotic cells and the ratio of Bax to Bcl-2 between DM(1) group and CON group. |
| 1504 | 18991018 | The number of TUNEL positive cells and Bax to Bcl-2 ratio was partially reversed in DM(2) group. |
| 1505 | 18991018 | But glucose control had no effect on the apoptotic cells and the expression of Bax and Bcl-2 in DM(3) group. |
| 1506 | 18991018 | There was a positive correlation between apoptotic cells and Bax/Bcl-2 ratio in the retina (r = 0.808, P < 0.01). |
| 1507 | 18991018 | Good blood glucose control at early stage can decrease the number of apoptotic cells in the retina; the decreased apoptosis is correlated with the down-regulation of Bax to Bcl-2 ratio. |
| 1508 | 18991018 | The timing of re-institution of good blood glucose control affects apoptosis and expression of Bax and Bcl-2 in the retina of diabetic rats. |
| 1509 | 18991018 | We explored the effect of re-institution of good blood glucose control on apoptosis and apoptosis related genes (Bax and Bcl-2) in the retina of diabetic rats. |
| 1510 | 18991018 | Expression of Bax and Bcl-2 in the retina was studied by immunohistochemistry and the apoptotic cells were stained using the TUNEL method. |
| 1511 | 18991018 | The apoptotic cell, expression of Bax and Bcl-2 and the ratio of Bax to Bcl-2 in the retina was increased in DM group compared with normal rats' (P < 0.01). |
| 1512 | 18991018 | There was no significant difference in apoptotic cells and the ratio of Bax to Bcl-2 between DM(1) group and CON group. |
| 1513 | 18991018 | The number of TUNEL positive cells and Bax to Bcl-2 ratio was partially reversed in DM(2) group. |
| 1514 | 18991018 | But glucose control had no effect on the apoptotic cells and the expression of Bax and Bcl-2 in DM(3) group. |
| 1515 | 18991018 | There was a positive correlation between apoptotic cells and Bax/Bcl-2 ratio in the retina (r = 0.808, P < 0.01). |
| 1516 | 18991018 | Good blood glucose control at early stage can decrease the number of apoptotic cells in the retina; the decreased apoptosis is correlated with the down-regulation of Bax to Bcl-2 ratio. |
| 1517 | 18991018 | The timing of re-institution of good blood glucose control affects apoptosis and expression of Bax and Bcl-2 in the retina of diabetic rats. |
| 1518 | 18991018 | We explored the effect of re-institution of good blood glucose control on apoptosis and apoptosis related genes (Bax and Bcl-2) in the retina of diabetic rats. |
| 1519 | 18991018 | Expression of Bax and Bcl-2 in the retina was studied by immunohistochemistry and the apoptotic cells were stained using the TUNEL method. |
| 1520 | 18991018 | The apoptotic cell, expression of Bax and Bcl-2 and the ratio of Bax to Bcl-2 in the retina was increased in DM group compared with normal rats' (P < 0.01). |
| 1521 | 18991018 | There was no significant difference in apoptotic cells and the ratio of Bax to Bcl-2 between DM(1) group and CON group. |
| 1522 | 18991018 | The number of TUNEL positive cells and Bax to Bcl-2 ratio was partially reversed in DM(2) group. |
| 1523 | 18991018 | But glucose control had no effect on the apoptotic cells and the expression of Bax and Bcl-2 in DM(3) group. |
| 1524 | 18991018 | There was a positive correlation between apoptotic cells and Bax/Bcl-2 ratio in the retina (r = 0.808, P < 0.01). |
| 1525 | 18991018 | Good blood glucose control at early stage can decrease the number of apoptotic cells in the retina; the decreased apoptosis is correlated with the down-regulation of Bax to Bcl-2 ratio. |
| 1526 | 18991018 | The timing of re-institution of good blood glucose control affects apoptosis and expression of Bax and Bcl-2 in the retina of diabetic rats. |
| 1527 | 18991018 | We explored the effect of re-institution of good blood glucose control on apoptosis and apoptosis related genes (Bax and Bcl-2) in the retina of diabetic rats. |
| 1528 | 18991018 | Expression of Bax and Bcl-2 in the retina was studied by immunohistochemistry and the apoptotic cells were stained using the TUNEL method. |
| 1529 | 18991018 | The apoptotic cell, expression of Bax and Bcl-2 and the ratio of Bax to Bcl-2 in the retina was increased in DM group compared with normal rats' (P < 0.01). |
| 1530 | 18991018 | There was no significant difference in apoptotic cells and the ratio of Bax to Bcl-2 between DM(1) group and CON group. |
| 1531 | 18991018 | The number of TUNEL positive cells and Bax to Bcl-2 ratio was partially reversed in DM(2) group. |
| 1532 | 18991018 | But glucose control had no effect on the apoptotic cells and the expression of Bax and Bcl-2 in DM(3) group. |
| 1533 | 18991018 | There was a positive correlation between apoptotic cells and Bax/Bcl-2 ratio in the retina (r = 0.808, P < 0.01). |
| 1534 | 18991018 | Good blood glucose control at early stage can decrease the number of apoptotic cells in the retina; the decreased apoptosis is correlated with the down-regulation of Bax to Bcl-2 ratio. |