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Gene Information
Gene symbol: TNFRSF11B
Gene name: tumor necrosis factor receptor superfamily, member 11b
HGNC ID: 11909
Synonyms: OCIF, TR1
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 14504275 | Teriparatide (human parathyroid hormone (1-34)) inhibits osteogenic vascular calcification in diabetic low density lipoprotein receptor-deficient mice. |
| 2 | 14504275 | We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. |
| 3 | 14504275 | LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week. |
| 4 | 14504275 | PTH(1-34) increased bone mineral content (by dual energy x-ray absorptiometry) in LDLR -/- mice, with induction of osseous osteopontin (OPN) expression and serum OPN levels (>150 nM); PTH(1-34) did not significantly change serum glucose, lipids, body weight, or fat mass. |
| 5 | 14504275 | PTH(1-34) suppressed aortic OPN and Msx2 expression >50% and decreased cardiac valve calcification 80% (8.3 +/- 1.5% versus 1.4 +/- 0.5%; p < 0.001). |
| 6 | 14504275 | Of the known circulating regulators of vascular calcification (OPN, osteoprotegerin, and leptin), PTH(1-34) regulated only serum OPN. |
| 7 | 14504275 | We therefore studied actions of PTH(1-34) and OPN in vitro on cells induced to mineralize with Msx2. |
| 8 | 14504275 | PTH(1-34) inhibits vascular calcification and aortic osteogenic differentiation via direct actions and potentially via circulating OPN. |
| 9 | 14661073 | We measured BMD by dual-energy X-ray absorptiometry (DXA) and quantitative bone ultrasound (QUS), as well as the serum levels of osteocalcin (OC), bone-specific alkaline phosphatase (BAP), osteoprotegerin (OPG) and its ligand RANKL, and the urinary concentration of the C-terminal telopeptides of type I collagen (CrossLaps), in 36 patient (20 male and 16 female) with serious atherosclerotic involvement of the carotid and/or femoral artery to investigate the underlying mechanism of vascular and osseous disorders. |
| 10 | 15102615 | Current data suggest that paracrine signals are provided by bone morphogenetic protein-2, Wnts, parathyroid hormone-related polypeptide, osteopontin, osteoprotegerin, and matrix Gla protein, all entrained to endocrine, metabolic, inflammatory, and mechanical cues. |
| 11 | 15292354 | Localization of osteoprotegerin, tumor necrosis factor-related apoptosis-inducing ligand, and receptor activator of nuclear factor-kappaB ligand in Mönckeberg's sclerosis and atherosclerosis. |
| 12 | 15292354 | Of note, TNF-related apoptosis-inducing ligand, an inducer of apoptosis that is also blocked by OPG, displayed a similar spatial distribution as OPG. |
| 13 | 15292354 | In summary, we demonstrate enhanced apoptosis adjacent to vascular calcification, and the concurrent expression of regulators of apoptosis and osteoclastic differentiation, TNF-related apoptosis-inducing ligand and OPG, suggesting their involvement in the pathogenesis of vascular calcification. |
| 14 | 15292354 | Localization of osteoprotegerin, tumor necrosis factor-related apoptosis-inducing ligand, and receptor activator of nuclear factor-kappaB ligand in Mönckeberg's sclerosis and atherosclerosis. |
| 15 | 15292354 | Of note, TNF-related apoptosis-inducing ligand, an inducer of apoptosis that is also blocked by OPG, displayed a similar spatial distribution as OPG. |
| 16 | 15292354 | In summary, we demonstrate enhanced apoptosis adjacent to vascular calcification, and the concurrent expression of regulators of apoptosis and osteoclastic differentiation, TNF-related apoptosis-inducing ligand and OPG, suggesting their involvement in the pathogenesis of vascular calcification. |
| 17 | 15292354 | Localization of osteoprotegerin, tumor necrosis factor-related apoptosis-inducing ligand, and receptor activator of nuclear factor-kappaB ligand in Mönckeberg's sclerosis and atherosclerosis. |
| 18 | 15292354 | Of note, TNF-related apoptosis-inducing ligand, an inducer of apoptosis that is also blocked by OPG, displayed a similar spatial distribution as OPG. |
| 19 | 15292354 | In summary, we demonstrate enhanced apoptosis adjacent to vascular calcification, and the concurrent expression of regulators of apoptosis and osteoclastic differentiation, TNF-related apoptosis-inducing ligand and OPG, suggesting their involvement in the pathogenesis of vascular calcification. |
| 20 | 15322748 | However, the recent recognition that the receptor activator of nuclear factor kappa B ligand (RANK-L)/osteoprotegerin (OPG) signalling pathway is central to the processes regulating bone turnover in a wide variety of medical conditions has raised the possibility that the same cytokines may be involved in the osteolysis which accompanies diabetic neuropathy. |
| 21 | 15322748 | This is made more likely by the realisation that the RANK-L/OPG pathway is also thought to mediate the calcification of vascular smooth muscle cells in coronary and peripheral vascular disease. |
| 22 | 15322748 | However, the recent recognition that the receptor activator of nuclear factor kappa B ligand (RANK-L)/osteoprotegerin (OPG) signalling pathway is central to the processes regulating bone turnover in a wide variety of medical conditions has raised the possibility that the same cytokines may be involved in the osteolysis which accompanies diabetic neuropathy. |
| 23 | 15322748 | This is made more likely by the realisation that the RANK-L/OPG pathway is also thought to mediate the calcification of vascular smooth muscle cells in coronary and peripheral vascular disease. |
| 24 | 15564564 | Regulation of vascular calcification by osteoclast regulatory factors RANKL and osteoprotegerin. |
| 25 | 15564564 | One emerging area in vascular biology involves the RANKL/RANK/OPG system, molecules of the tumor necrosis factor-related family recently discovered to be critical regulators of immune and skeletal biology. |
| 26 | 15564564 | Concerted research efforts are greatly needed to understand these potential roles, clarify whether RANKL (receptor activator of nuclear factor kappaB ligand) promotes and osteoprotegerin (OPG) protects against vascular calcification, define how OPG genetic polymorphisms relate to cardiovascular disease, and learn whether elevated serum OPG levels reflect endothelial dysfunction in patients. |
| 27 | 15564564 | Overall, the RANKL/RANK/OPG system may mediate important and complex links between the vascular, skeletal, and immune systems. |
| 28 | 15564564 | Regulation of vascular calcification by osteoclast regulatory factors RANKL and osteoprotegerin. |
| 29 | 15564564 | One emerging area in vascular biology involves the RANKL/RANK/OPG system, molecules of the tumor necrosis factor-related family recently discovered to be critical regulators of immune and skeletal biology. |
| 30 | 15564564 | Concerted research efforts are greatly needed to understand these potential roles, clarify whether RANKL (receptor activator of nuclear factor kappaB ligand) promotes and osteoprotegerin (OPG) protects against vascular calcification, define how OPG genetic polymorphisms relate to cardiovascular disease, and learn whether elevated serum OPG levels reflect endothelial dysfunction in patients. |
| 31 | 15564564 | Overall, the RANKL/RANK/OPG system may mediate important and complex links between the vascular, skeletal, and immune systems. |
| 32 | 15576949 | Bone associated proteins including osteopontin, matrix Gla protein and osteoprotegerin may be involved in the progression of atherosclerosis. |
| 33 | 15700136 | Arterial osteoprotegerin: increased amounts in diabetes and modifiable synthesis from vascular smooth muscle cells by insulin and TNF-alpha. |
| 34 | 15855336 | When diabetic mice are treated with the RANKL antagonist osteoprotegerin (OPG), there is a significant reversal of alveolar bone loss, as well as reduced RANKL expression in A. actinomycetemcomitans-reactive CD4+ T-cells. |
| 35 | 15855336 | Thus, microorganism-reactive CD4+ T-cells and the RANKL-OPG axis provide the molecular basis of the advanced periodontal breakdown in diabetes and, therefore, OPG may hold therapeutic potential for treating bone loss in diabetic subjects at high risk. |
| 36 | 15855336 | When diabetic mice are treated with the RANKL antagonist osteoprotegerin (OPG), there is a significant reversal of alveolar bone loss, as well as reduced RANKL expression in A. actinomycetemcomitans-reactive CD4+ T-cells. |
| 37 | 15855336 | Thus, microorganism-reactive CD4+ T-cells and the RANKL-OPG axis provide the molecular basis of the advanced periodontal breakdown in diabetes and, therefore, OPG may hold therapeutic potential for treating bone loss in diabetic subjects at high risk. |
| 38 | 15860239 | To clarify the pathogenesis of altered bone metabolism in diabetic state and its underlying mechanisms, the bone mineral content and fasting levels of serum intact parathyroid hormone (i-PTH), intact osteocalcin (i-OC), tartrate-resistant acid phosphatase (TRAP) and osteoclastgenesis inhibitory factor/osteoprotegerin (OCIF/OPG) were measured in male type 2 diabetic patients and their age-matched controls. |
| 39 | 15860239 | In addition, urine levels of osteoclastic markers, C-telopeptide of type I collagen (CTx), deoxypyridinoline (DPD), and N-telopeptide of type I collagen (NTx) were simultaneously determined. |
| 40 | 15860239 | It was also observed that urinary excretion of CTx, DPD, and NTx was significantly increased in the diabetics as compared with the controls. |
| 41 | 15860239 | Unexpectedly, serum levels of OCIF/OPG tended to be higher in the diabetic group, and these values exhibited a significantly positive correlation with those of serum TRAP. |
| 42 | 15860239 | There was found a significantly negative correlation between serum TRAP and bone mineral density (BMD) and also between serum OCIF/OPG and bone mineral density. |
| 43 | 15860239 | To clarify the pathogenesis of altered bone metabolism in diabetic state and its underlying mechanisms, the bone mineral content and fasting levels of serum intact parathyroid hormone (i-PTH), intact osteocalcin (i-OC), tartrate-resistant acid phosphatase (TRAP) and osteoclastgenesis inhibitory factor/osteoprotegerin (OCIF/OPG) were measured in male type 2 diabetic patients and their age-matched controls. |
| 44 | 15860239 | In addition, urine levels of osteoclastic markers, C-telopeptide of type I collagen (CTx), deoxypyridinoline (DPD), and N-telopeptide of type I collagen (NTx) were simultaneously determined. |
| 45 | 15860239 | It was also observed that urinary excretion of CTx, DPD, and NTx was significantly increased in the diabetics as compared with the controls. |
| 46 | 15860239 | Unexpectedly, serum levels of OCIF/OPG tended to be higher in the diabetic group, and these values exhibited a significantly positive correlation with those of serum TRAP. |
| 47 | 15860239 | There was found a significantly negative correlation between serum TRAP and bone mineral density (BMD) and also between serum OCIF/OPG and bone mineral density. |
| 48 | 15860239 | To clarify the pathogenesis of altered bone metabolism in diabetic state and its underlying mechanisms, the bone mineral content and fasting levels of serum intact parathyroid hormone (i-PTH), intact osteocalcin (i-OC), tartrate-resistant acid phosphatase (TRAP) and osteoclastgenesis inhibitory factor/osteoprotegerin (OCIF/OPG) were measured in male type 2 diabetic patients and their age-matched controls. |
| 49 | 15860239 | In addition, urine levels of osteoclastic markers, C-telopeptide of type I collagen (CTx), deoxypyridinoline (DPD), and N-telopeptide of type I collagen (NTx) were simultaneously determined. |
| 50 | 15860239 | It was also observed that urinary excretion of CTx, DPD, and NTx was significantly increased in the diabetics as compared with the controls. |
| 51 | 15860239 | Unexpectedly, serum levels of OCIF/OPG tended to be higher in the diabetic group, and these values exhibited a significantly positive correlation with those of serum TRAP. |
| 52 | 15860239 | There was found a significantly negative correlation between serum TRAP and bone mineral density (BMD) and also between serum OCIF/OPG and bone mineral density. |
| 53 | 15936463 | The relationship between insulin resistance assessed by HOMA-IR and serum osteoprotegerin levels in obesity. |
| 54 | 16362152 | Dysregulations of calcification inhibitors, including fetuin-A, matrix Gla protein, osteoprotegerin, and pyrophosphates may also be pathophysiologically relevant factors in the context of uremic extraosseous calcification. |
| 55 | 16408509 | Besides apoptosis and Pi uptake, such proteins as osteoprotegerin (OPG), matrix Gla protein (MGP), Klotho, fetuin-A, and apoE have been shown to negatively affect vascular calcification. |
| 56 | 16408509 | Many previous reports suggest that vascular calcification appears to be regulated by promoting factors, such as Pi, apoptosis, modified LDL, advanced glycation end products, oxidative stress, vitaminD3, glucocorticoid, cbfa-1, osteopontin, and inhibitory factors, such as OPG, MGP, Klotho, fetuin-A, PTH/PTHrP, pyrophosphate, statins, and bisphosphonates. |
| 57 | 16408509 | Besides apoptosis and Pi uptake, such proteins as osteoprotegerin (OPG), matrix Gla protein (MGP), Klotho, fetuin-A, and apoE have been shown to negatively affect vascular calcification. |
| 58 | 16408509 | Many previous reports suggest that vascular calcification appears to be regulated by promoting factors, such as Pi, apoptosis, modified LDL, advanced glycation end products, oxidative stress, vitaminD3, glucocorticoid, cbfa-1, osteopontin, and inhibitory factors, such as OPG, MGP, Klotho, fetuin-A, PTH/PTHrP, pyrophosphate, statins, and bisphosphonates. |
| 59 | 16549048 | Dehydroepiandrosterone inhibited the bone resorption through the upregulation of OPG/RANKL. |
| 60 | 16549048 | Having isolated and cultured osteoblasts (OBs) and osteoclasts (OCs), we analysed the effect of DHEA on osteoblastic viability, regulation of DHEA on the expression of osteoprotegerin (OPG)/receptor activator of NF-kappaB ligand (RANKL) mRNA in OBs, and then observed the action of DHEA on bone resorption of OCs in the presence or absence of OBs. |
| 61 | 16549048 | DHEA could apparently increase the ratio of OPG/RANKL mRNA in OBs. |
| 62 | 16549048 | We concluded, therefore, only in the presence of OBs, DHEA could inhibit the bone resorption of OCs, which may be mediated by OPG/RANKL of OBs. |
| 63 | 16549048 | Dehydroepiandrosterone inhibited the bone resorption through the upregulation of OPG/RANKL. |
| 64 | 16549048 | Having isolated and cultured osteoblasts (OBs) and osteoclasts (OCs), we analysed the effect of DHEA on osteoblastic viability, regulation of DHEA on the expression of osteoprotegerin (OPG)/receptor activator of NF-kappaB ligand (RANKL) mRNA in OBs, and then observed the action of DHEA on bone resorption of OCs in the presence or absence of OBs. |
| 65 | 16549048 | DHEA could apparently increase the ratio of OPG/RANKL mRNA in OBs. |
| 66 | 16549048 | We concluded, therefore, only in the presence of OBs, DHEA could inhibit the bone resorption of OCs, which may be mediated by OPG/RANKL of OBs. |
| 67 | 16549048 | Dehydroepiandrosterone inhibited the bone resorption through the upregulation of OPG/RANKL. |
| 68 | 16549048 | Having isolated and cultured osteoblasts (OBs) and osteoclasts (OCs), we analysed the effect of DHEA on osteoblastic viability, regulation of DHEA on the expression of osteoprotegerin (OPG)/receptor activator of NF-kappaB ligand (RANKL) mRNA in OBs, and then observed the action of DHEA on bone resorption of OCs in the presence or absence of OBs. |
| 69 | 16549048 | DHEA could apparently increase the ratio of OPG/RANKL mRNA in OBs. |
| 70 | 16549048 | We concluded, therefore, only in the presence of OBs, DHEA could inhibit the bone resorption of OCs, which may be mediated by OPG/RANKL of OBs. |
| 71 | 16549048 | Dehydroepiandrosterone inhibited the bone resorption through the upregulation of OPG/RANKL. |
| 72 | 16549048 | Having isolated and cultured osteoblasts (OBs) and osteoclasts (OCs), we analysed the effect of DHEA on osteoblastic viability, regulation of DHEA on the expression of osteoprotegerin (OPG)/receptor activator of NF-kappaB ligand (RANKL) mRNA in OBs, and then observed the action of DHEA on bone resorption of OCs in the presence or absence of OBs. |
| 73 | 16549048 | DHEA could apparently increase the ratio of OPG/RANKL mRNA in OBs. |
| 74 | 16549048 | We concluded, therefore, only in the presence of OBs, DHEA could inhibit the bone resorption of OCs, which may be mediated by OPG/RANKL of OBs. |
| 75 | 16687626 | The primary objectives of this analysis were to examine the effects of early posttransplantation (10 wk) serum levels of osteoprotegerin (OPG), mannose-binding lectin (MBL), and MBL-associated serine proteases (MASP; MASP-2 and MASP-3) on long-term (8-yr) patient survival, graft survival, and cardiovascular (CV) death. |
| 76 | 16687626 | Multiple linear regression analysis revealed that age, creatinine clearance, and high-sensitivity C-reactive protein all were independently associated with OPG (R2=0.42). |
| 77 | 16687626 | Serum levels of MBL, MASP-2, and MASP-3 were not significantly associated with patient survival, CV death, or graft loss. |
| 78 | 16687626 | The primary objectives of this analysis were to examine the effects of early posttransplantation (10 wk) serum levels of osteoprotegerin (OPG), mannose-binding lectin (MBL), and MBL-associated serine proteases (MASP; MASP-2 and MASP-3) on long-term (8-yr) patient survival, graft survival, and cardiovascular (CV) death. |
| 79 | 16687626 | Multiple linear regression analysis revealed that age, creatinine clearance, and high-sensitivity C-reactive protein all were independently associated with OPG (R2=0.42). |
| 80 | 16687626 | Serum levels of MBL, MASP-2, and MASP-3 were not significantly associated with patient survival, CV death, or graft loss. |
| 81 | 16804084 | In multivariate analysis, osteoprotegerin was significantly associated with endothelium-dependent arterial dilation, fasting blood glucose (FBG), HbA(1c) (A1C), and ultrasensitive C-reactive protein (CRP) at baseline (P < 0.01). |
| 82 | 16804084 | The absolute changes in osteoprotegerin showed significant correlation with changes in endothelium-dependent arterial dilation, FBG, A1C, and CRP in diabetic patients during the course of treatment (P < 0.01). |
| 83 | 16804084 | In multivariate analysis, osteoprotegerin was significantly associated with endothelium-dependent arterial dilation, fasting blood glucose (FBG), HbA(1c) (A1C), and ultrasensitive C-reactive protein (CRP) at baseline (P < 0.01). |
| 84 | 16804084 | The absolute changes in osteoprotegerin showed significant correlation with changes in endothelium-dependent arterial dilation, FBG, A1C, and CRP in diabetic patients during the course of treatment (P < 0.01). |
| 85 | 16918372 | The signaling axis constituted by osteoprotegerin (OPG), receptor activator nuclear factor kB (RANK) and its ligand (RANKL), along with the monocyte colony stimulating factor (M-CSF) and the transcription factor core Binding protein (Cbfa-1), play a pivotal role in the control of VC. |
| 86 | 16918372 | In contrast, fetuin-A, matrix G1a protein (MGP) and osteopontin (OPN) control the inhibition of VC. |
| 87 | 16918372 | The inflammatory cytokines interleukin (IL-1) and tumor necrosis factor (TNF)-alpha enhance OPG and RANKL function in the vessel wall leading to VC. |
| 88 | 16918372 | The signaling axis constituted by osteoprotegerin (OPG), receptor activator nuclear factor kB (RANK) and its ligand (RANKL), along with the monocyte colony stimulating factor (M-CSF) and the transcription factor core Binding protein (Cbfa-1), play a pivotal role in the control of VC. |
| 89 | 16918372 | In contrast, fetuin-A, matrix G1a protein (MGP) and osteopontin (OPN) control the inhibition of VC. |
| 90 | 16918372 | The inflammatory cytokines interleukin (IL-1) and tumor necrosis factor (TNF)-alpha enhance OPG and RANKL function in the vessel wall leading to VC. |
| 91 | 17023086 | Changes of osteoprotegerin before and after insulin therapy in type 1 diabetic patients. |
| 92 | 17046554 | Furthermore, mannose-binding lectin (P = .06), soluble intercellular adhesion molecule 1 (P = .08), and osteoprotegerin (P = .08) tended to be increased in relatives. |
| 93 | 17046554 | The following markers of endothelial function were comparable at baseline: FMD, C-reactive protein, plasminogen activator inhibitor 1, and soluble vascular cell adhesion molecule 1. |
| 94 | 17056676 | We examined the effects of insulin on calcifying smooth muscle cells in vitro and measured the expression of the bone-related molecule osteoprotegerin (OPG). |
| 95 | 17056676 | Histochemistry was used for determination of alkaline phosphatase (ALP). |
| 96 | 17056676 | Bone sialoprotein (BSP) and OPG mRNA expressions were done by RT-PCR. beta-Glycerophosphate was able to induce calcification in human smooth muscle cells from a series of donors after variable time in culture. |
| 97 | 17056676 | Calcified cells expressed ALP and BSP activity in high levels. |
| 98 | 17056676 | Effects of insulin and modulations by OPG on the calcification process in arterial cells may play a role in the development of calcifications as part of the diabetic macroangiopathy. |
| 99 | 17056676 | We examined the effects of insulin on calcifying smooth muscle cells in vitro and measured the expression of the bone-related molecule osteoprotegerin (OPG). |
| 100 | 17056676 | Histochemistry was used for determination of alkaline phosphatase (ALP). |
| 101 | 17056676 | Bone sialoprotein (BSP) and OPG mRNA expressions were done by RT-PCR. beta-Glycerophosphate was able to induce calcification in human smooth muscle cells from a series of donors after variable time in culture. |
| 102 | 17056676 | Calcified cells expressed ALP and BSP activity in high levels. |
| 103 | 17056676 | Effects of insulin and modulations by OPG on the calcification process in arterial cells may play a role in the development of calcifications as part of the diabetic macroangiopathy. |
| 104 | 17056676 | We examined the effects of insulin on calcifying smooth muscle cells in vitro and measured the expression of the bone-related molecule osteoprotegerin (OPG). |
| 105 | 17056676 | Histochemistry was used for determination of alkaline phosphatase (ALP). |
| 106 | 17056676 | Bone sialoprotein (BSP) and OPG mRNA expressions were done by RT-PCR. beta-Glycerophosphate was able to induce calcification in human smooth muscle cells from a series of donors after variable time in culture. |
| 107 | 17056676 | Calcified cells expressed ALP and BSP activity in high levels. |
| 108 | 17056676 | Effects of insulin and modulations by OPG on the calcification process in arterial cells may play a role in the development of calcifications as part of the diabetic macroangiopathy. |
| 109 | 17148684 | Serum levels of OPG, but not of its cognate ligand receptor activator of nuclear factor-kappaB ligand (RANKL), were significantly increased in type 2 diabetes mellitus patients compared with healthy blood donors. |
| 110 | 17148684 | Serum OPG increased early after diabetes induction in both mouse strains and showed a positive correlation with blood glucose levels and an inverse correlation with the levels of free (OPG-unbound) RANKL. |
| 111 | 17148684 | The in vitro addition of tumor necrosis factor-alpha to human vascular endothelial cells, but not human peripheral blood mononuclear cells, markedly enhanced OPG release in culture. |
| 112 | 17148684 | In contrast, high glucose concentrations did not modulate OPG release when used alone or in association with tumor necrosis factor-alpha. |
| 113 | 17148684 | Moreover, the ability of soluble RANKL to activate the extracellular signal-regulated kinase/mitogen-activated protein kinase and endothelial nitric-oxide synthase pathways in endothelial cells was neutralized by preincubation with recombinant OPG. |
| 114 | 17148684 | Serum levels of OPG, but not of its cognate ligand receptor activator of nuclear factor-kappaB ligand (RANKL), were significantly increased in type 2 diabetes mellitus patients compared with healthy blood donors. |
| 115 | 17148684 | Serum OPG increased early after diabetes induction in both mouse strains and showed a positive correlation with blood glucose levels and an inverse correlation with the levels of free (OPG-unbound) RANKL. |
| 116 | 17148684 | The in vitro addition of tumor necrosis factor-alpha to human vascular endothelial cells, but not human peripheral blood mononuclear cells, markedly enhanced OPG release in culture. |
| 117 | 17148684 | In contrast, high glucose concentrations did not modulate OPG release when used alone or in association with tumor necrosis factor-alpha. |
| 118 | 17148684 | Moreover, the ability of soluble RANKL to activate the extracellular signal-regulated kinase/mitogen-activated protein kinase and endothelial nitric-oxide synthase pathways in endothelial cells was neutralized by preincubation with recombinant OPG. |
| 119 | 17148684 | Serum levels of OPG, but not of its cognate ligand receptor activator of nuclear factor-kappaB ligand (RANKL), were significantly increased in type 2 diabetes mellitus patients compared with healthy blood donors. |
| 120 | 17148684 | Serum OPG increased early after diabetes induction in both mouse strains and showed a positive correlation with blood glucose levels and an inverse correlation with the levels of free (OPG-unbound) RANKL. |
| 121 | 17148684 | The in vitro addition of tumor necrosis factor-alpha to human vascular endothelial cells, but not human peripheral blood mononuclear cells, markedly enhanced OPG release in culture. |
| 122 | 17148684 | In contrast, high glucose concentrations did not modulate OPG release when used alone or in association with tumor necrosis factor-alpha. |
| 123 | 17148684 | Moreover, the ability of soluble RANKL to activate the extracellular signal-regulated kinase/mitogen-activated protein kinase and endothelial nitric-oxide synthase pathways in endothelial cells was neutralized by preincubation with recombinant OPG. |
| 124 | 17148684 | Serum levels of OPG, but not of its cognate ligand receptor activator of nuclear factor-kappaB ligand (RANKL), were significantly increased in type 2 diabetes mellitus patients compared with healthy blood donors. |
| 125 | 17148684 | Serum OPG increased early after diabetes induction in both mouse strains and showed a positive correlation with blood glucose levels and an inverse correlation with the levels of free (OPG-unbound) RANKL. |
| 126 | 17148684 | The in vitro addition of tumor necrosis factor-alpha to human vascular endothelial cells, but not human peripheral blood mononuclear cells, markedly enhanced OPG release in culture. |
| 127 | 17148684 | In contrast, high glucose concentrations did not modulate OPG release when used alone or in association with tumor necrosis factor-alpha. |
| 128 | 17148684 | Moreover, the ability of soluble RANKL to activate the extracellular signal-regulated kinase/mitogen-activated protein kinase and endothelial nitric-oxide synthase pathways in endothelial cells was neutralized by preincubation with recombinant OPG. |
| 129 | 17148684 | Serum levels of OPG, but not of its cognate ligand receptor activator of nuclear factor-kappaB ligand (RANKL), were significantly increased in type 2 diabetes mellitus patients compared with healthy blood donors. |
| 130 | 17148684 | Serum OPG increased early after diabetes induction in both mouse strains and showed a positive correlation with blood glucose levels and an inverse correlation with the levels of free (OPG-unbound) RANKL. |
| 131 | 17148684 | The in vitro addition of tumor necrosis factor-alpha to human vascular endothelial cells, but not human peripheral blood mononuclear cells, markedly enhanced OPG release in culture. |
| 132 | 17148684 | In contrast, high glucose concentrations did not modulate OPG release when used alone or in association with tumor necrosis factor-alpha. |
| 133 | 17148684 | Moreover, the ability of soluble RANKL to activate the extracellular signal-regulated kinase/mitogen-activated protein kinase and endothelial nitric-oxide synthase pathways in endothelial cells was neutralized by preincubation with recombinant OPG. |
| 134 | 17284635 | Sporadic hyperphosphatasia syndrome featuring periostitis and accelerated skeletal turnover without receptor activator of nuclear factor-kappaB, osteoprotegerin, or sequestosome-1 gene defects. |
| 135 | 17293196 | Multivariable logistic regression was used to assess associations among OPG, cardiovascular risk factors, CAC, and aortic plaque. |
| 136 | 17293196 | Age, female gender, black race, smoking, personal and family history of coronary artery disease (CAD), diabetes mellitus, hyperlipidemia, CAC, and aortic plaque were significantly associated with higher plasma OPG levels (p <0.01) in univariable analyses. |
| 137 | 17293196 | The prevalence of CAC and aortic plaque increased across OPG quartiles (p <0.001 for each). |
| 138 | 17293196 | An OPG level in the fourth quartile was independently associated with CAC (RR 1.39, 95% confidence interval 1.01 to 1.93) and aortic plaque (RR 1.42, 95% confidence interval 1.09 to 1.86) after adjustment for age, gender, smoking, diabetes, hyperlipidemia, and family history of premature CAD. |
| 139 | 17293196 | In conclusion, plasma OPG is independently associated with CAC and aortic plaque in an unselected population, suggesting it may be a novel biomarker for atherosclerosis in humans. |
| 140 | 17293196 | Multivariable logistic regression was used to assess associations among OPG, cardiovascular risk factors, CAC, and aortic plaque. |
| 141 | 17293196 | Age, female gender, black race, smoking, personal and family history of coronary artery disease (CAD), diabetes mellitus, hyperlipidemia, CAC, and aortic plaque were significantly associated with higher plasma OPG levels (p <0.01) in univariable analyses. |
| 142 | 17293196 | The prevalence of CAC and aortic plaque increased across OPG quartiles (p <0.001 for each). |
| 143 | 17293196 | An OPG level in the fourth quartile was independently associated with CAC (RR 1.39, 95% confidence interval 1.01 to 1.93) and aortic plaque (RR 1.42, 95% confidence interval 1.09 to 1.86) after adjustment for age, gender, smoking, diabetes, hyperlipidemia, and family history of premature CAD. |
| 144 | 17293196 | In conclusion, plasma OPG is independently associated with CAC and aortic plaque in an unselected population, suggesting it may be a novel biomarker for atherosclerosis in humans. |
| 145 | 17293196 | Multivariable logistic regression was used to assess associations among OPG, cardiovascular risk factors, CAC, and aortic plaque. |
| 146 | 17293196 | Age, female gender, black race, smoking, personal and family history of coronary artery disease (CAD), diabetes mellitus, hyperlipidemia, CAC, and aortic plaque were significantly associated with higher plasma OPG levels (p <0.01) in univariable analyses. |
| 147 | 17293196 | The prevalence of CAC and aortic plaque increased across OPG quartiles (p <0.001 for each). |
| 148 | 17293196 | An OPG level in the fourth quartile was independently associated with CAC (RR 1.39, 95% confidence interval 1.01 to 1.93) and aortic plaque (RR 1.42, 95% confidence interval 1.09 to 1.86) after adjustment for age, gender, smoking, diabetes, hyperlipidemia, and family history of premature CAD. |
| 149 | 17293196 | In conclusion, plasma OPG is independently associated with CAC and aortic plaque in an unselected population, suggesting it may be a novel biomarker for atherosclerosis in humans. |
| 150 | 17293196 | Multivariable logistic regression was used to assess associations among OPG, cardiovascular risk factors, CAC, and aortic plaque. |
| 151 | 17293196 | Age, female gender, black race, smoking, personal and family history of coronary artery disease (CAD), diabetes mellitus, hyperlipidemia, CAC, and aortic plaque were significantly associated with higher plasma OPG levels (p <0.01) in univariable analyses. |
| 152 | 17293196 | The prevalence of CAC and aortic plaque increased across OPG quartiles (p <0.001 for each). |
| 153 | 17293196 | An OPG level in the fourth quartile was independently associated with CAC (RR 1.39, 95% confidence interval 1.01 to 1.93) and aortic plaque (RR 1.42, 95% confidence interval 1.09 to 1.86) after adjustment for age, gender, smoking, diabetes, hyperlipidemia, and family history of premature CAD. |
| 154 | 17293196 | In conclusion, plasma OPG is independently associated with CAC and aortic plaque in an unselected population, suggesting it may be a novel biomarker for atherosclerosis in humans. |
| 155 | 17293196 | Multivariable logistic regression was used to assess associations among OPG, cardiovascular risk factors, CAC, and aortic plaque. |
| 156 | 17293196 | Age, female gender, black race, smoking, personal and family history of coronary artery disease (CAD), diabetes mellitus, hyperlipidemia, CAC, and aortic plaque were significantly associated with higher plasma OPG levels (p <0.01) in univariable analyses. |
| 157 | 17293196 | The prevalence of CAC and aortic plaque increased across OPG quartiles (p <0.001 for each). |
| 158 | 17293196 | An OPG level in the fourth quartile was independently associated with CAC (RR 1.39, 95% confidence interval 1.01 to 1.93) and aortic plaque (RR 1.42, 95% confidence interval 1.09 to 1.86) after adjustment for age, gender, smoking, diabetes, hyperlipidemia, and family history of premature CAD. |
| 159 | 17293196 | In conclusion, plasma OPG is independently associated with CAC and aortic plaque in an unselected population, suggesting it may be a novel biomarker for atherosclerosis in humans. |
| 160 | 17443309 | Cytokine-induced osteoprotegerin expression protects pancreatic beta cells through p38 mitogen-activated protein kinase signalling against cell death. |
| 161 | 17550963 | The circadian rhythm of osteoprotegerin and its association with parathyroid hormone secretion. |
| 162 | 17556308 | In the spectrum of substances involved in the regulation of the process of soft-tissue calcification, the most extensively studied in the nephrology literature are bone morphogenetic protein 7, osteoprotegerin, matrix Gla protein, fetuin-A, and the phosphatonins. |
| 163 | 17686254 | [Changes of osteoprotegerin before and after insulin therapy in type 1 diabetic patients]. |
| 164 | 17878722 | Polymorphisms at the osteoprotegerin and interleukin-6 genes in relation to first-ever stroke. |
| 165 | 17897105 | Aortic pulse wave velocity (PWV), augmentation index (AIx), and levels of inhibitors of vascular calcification (fetuin-A, matrix-GLA-protein, osteoprotegerin/RANKL) were measured at baseline and at the end of follow-up, and the differences between the groups were compared. |
| 166 | 17992602 | In this study, we evaluated the effect of BMP-2, BMP-7 and transforming growth factor beta (TGF-beta1) on the secretion and mRNA expression of OPG and its ligands receptor activator of nuclear factor-kappabeta ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL) in HVSMC. |
| 167 | 17992602 | RANKL mRNA expression declined when treated with TGF-beta1 but were increased by both BMPs. |
| 168 | 17992602 | TGF-beta1, BMP-2 and BMP-7 exert effects on OPG and its ligands, indicating that these peptides may be involved in the development of vascular calcifications. |
| 169 | 17992602 | In this study, we evaluated the effect of BMP-2, BMP-7 and transforming growth factor beta (TGF-beta1) on the secretion and mRNA expression of OPG and its ligands receptor activator of nuclear factor-kappabeta ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL) in HVSMC. |
| 170 | 17992602 | RANKL mRNA expression declined when treated with TGF-beta1 but were increased by both BMPs. |
| 171 | 17992602 | TGF-beta1, BMP-2 and BMP-7 exert effects on OPG and its ligands, indicating that these peptides may be involved in the development of vascular calcifications. |
| 172 | 18165109 | The association of the active phase of the disease with inflammation, increasing osteopenia, and increasing calcification of the arterial walls strongly suggests, however, the involvement of the receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) cytokine pathway, which is closely involved in all three processes. |
| 173 | 18165109 | The evidence for increased expression of RANKL and OPG in diabetes and neuropathy as well as its potential significance is reviewed. |
| 174 | 18165109 | The association of the active phase of the disease with inflammation, increasing osteopenia, and increasing calcification of the arterial walls strongly suggests, however, the involvement of the receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) cytokine pathway, which is closely involved in all three processes. |
| 175 | 18165109 | The evidence for increased expression of RANKL and OPG in diabetes and neuropathy as well as its potential significance is reviewed. |
| 176 | 18202319 | TG2(-/-) SMCs lost the capacity for P(i) donor-induced formation of multicellular bone-like nodules and for increased expression of the type III sodium-dependent P(i) cotransporter Pit-1 and certain osteoblast and chondrocyte genes (tissue-nonspecific alkaline phosphatase, the osteoblast master transcription factor runx2, and chondrocyte-restricted aggrecan), and for P(i) donor- and bone morphogenetic protein-2-induced calcification. |
| 177 | 18202319 | Uniquely in TG2(-/-) SMCs, P(i) donor treatment increased expression of the physiological SMC chondro-osseous differentiation and calcification inhibitors osteoprotegerin, matrix Gla protein, and osteopontin. |
| 178 | 18202319 | TG2 expression also drove P(i)-stimulated calcification of mouse aortic ring organ cultures, which was suppressed by the TG2 catalytic site-specific inhibitor Boc-DON-Gln-Ile-Val-OMe (10 micromol/L). |
| 179 | 18202319 | Our results suggest that TG2 release in injured arteries is critical for programming chondro-osseous SMC differentiation and calcification in response to increased P(i) and bone morphogenetic protein-2. |
| 180 | 18287563 | Among those that showed the greatest changes in regulation were two death receptors, OPG (the gene encoding osteoprotegerin) and Fas, and the death ligand TRAIL. |
| 181 | 18299469 | Osteoprotegerin in relation to body weight, lipid parameters insulin sensitivity, adipocytokines, and C-reactive protein in obese and non-obese young individuals: results from both cross-sectional and interventional study. |
| 182 | 18393327 | Recent advances in understanding the mechanisms underlying the pathogenesis of osteopenia and osteoporosis and the central role of the RANKL/OPG signalling system have, however, suggested the possible involvement of other factors in the evolution of the disease. |
| 183 | 18393327 | The likely central role for the RANKL/OPG pathway suggests new possibilities for future treatments. |
| 184 | 18393327 | Recent advances in understanding the mechanisms underlying the pathogenesis of osteopenia and osteoporosis and the central role of the RANKL/OPG signalling system have, however, suggested the possible involvement of other factors in the evolution of the disease. |
| 185 | 18393327 | The likely central role for the RANKL/OPG pathway suggests new possibilities for future treatments. |
| 186 | 18592139 | Imbalance of RANK, RANKL and OPG expression during tibial fracture repair in diabetic rats. |
| 187 | 18592139 | To clarify the mechanisms of altered bone repair in the diabetic state, we investigated RANK, RANKL and OPG expression by immunohistochemistry and RT-PCR in the fracture sites of rats that were either healthy or made diabetic by alloxan. |
| 188 | 18592139 | The number of RANK, RANKL and OPG positive cells was decreased in the db group; however, the RANKL/OPG ratio was similar in controls and db at this time. |
| 189 | 18592139 | At day 14, numbers of RANKL and OPG positive cells and the mRNA expression for these markers were higher in the control group than in db (P = 0.008). |
| 190 | 18592139 | The RANKL/OPG ratio in the db group was greater than in controls. |
| 191 | 18592139 | Our results demonstrate an imbalance of RANKL/OPG expression associated with diabetes that may contribute to the delay of fracture repair during the course of diabetes. |
| 192 | 18592139 | Imbalance of RANK, RANKL and OPG expression during tibial fracture repair in diabetic rats. |
| 193 | 18592139 | To clarify the mechanisms of altered bone repair in the diabetic state, we investigated RANK, RANKL and OPG expression by immunohistochemistry and RT-PCR in the fracture sites of rats that were either healthy or made diabetic by alloxan. |
| 194 | 18592139 | The number of RANK, RANKL and OPG positive cells was decreased in the db group; however, the RANKL/OPG ratio was similar in controls and db at this time. |
| 195 | 18592139 | At day 14, numbers of RANKL and OPG positive cells and the mRNA expression for these markers were higher in the control group than in db (P = 0.008). |
| 196 | 18592139 | The RANKL/OPG ratio in the db group was greater than in controls. |
| 197 | 18592139 | Our results demonstrate an imbalance of RANKL/OPG expression associated with diabetes that may contribute to the delay of fracture repair during the course of diabetes. |
| 198 | 18592139 | Imbalance of RANK, RANKL and OPG expression during tibial fracture repair in diabetic rats. |
| 199 | 18592139 | To clarify the mechanisms of altered bone repair in the diabetic state, we investigated RANK, RANKL and OPG expression by immunohistochemistry and RT-PCR in the fracture sites of rats that were either healthy or made diabetic by alloxan. |
| 200 | 18592139 | The number of RANK, RANKL and OPG positive cells was decreased in the db group; however, the RANKL/OPG ratio was similar in controls and db at this time. |
| 201 | 18592139 | At day 14, numbers of RANKL and OPG positive cells and the mRNA expression for these markers were higher in the control group than in db (P = 0.008). |
| 202 | 18592139 | The RANKL/OPG ratio in the db group was greater than in controls. |
| 203 | 18592139 | Our results demonstrate an imbalance of RANKL/OPG expression associated with diabetes that may contribute to the delay of fracture repair during the course of diabetes. |
| 204 | 18592139 | Imbalance of RANK, RANKL and OPG expression during tibial fracture repair in diabetic rats. |
| 205 | 18592139 | To clarify the mechanisms of altered bone repair in the diabetic state, we investigated RANK, RANKL and OPG expression by immunohistochemistry and RT-PCR in the fracture sites of rats that were either healthy or made diabetic by alloxan. |
| 206 | 18592139 | The number of RANK, RANKL and OPG positive cells was decreased in the db group; however, the RANKL/OPG ratio was similar in controls and db at this time. |
| 207 | 18592139 | At day 14, numbers of RANKL and OPG positive cells and the mRNA expression for these markers were higher in the control group than in db (P = 0.008). |
| 208 | 18592139 | The RANKL/OPG ratio in the db group was greater than in controls. |
| 209 | 18592139 | Our results demonstrate an imbalance of RANKL/OPG expression associated with diabetes that may contribute to the delay of fracture repair during the course of diabetes. |
| 210 | 18592139 | Imbalance of RANK, RANKL and OPG expression during tibial fracture repair in diabetic rats. |
| 211 | 18592139 | To clarify the mechanisms of altered bone repair in the diabetic state, we investigated RANK, RANKL and OPG expression by immunohistochemistry and RT-PCR in the fracture sites of rats that were either healthy or made diabetic by alloxan. |
| 212 | 18592139 | The number of RANK, RANKL and OPG positive cells was decreased in the db group; however, the RANKL/OPG ratio was similar in controls and db at this time. |
| 213 | 18592139 | At day 14, numbers of RANKL and OPG positive cells and the mRNA expression for these markers were higher in the control group than in db (P = 0.008). |
| 214 | 18592139 | The RANKL/OPG ratio in the db group was greater than in controls. |
| 215 | 18592139 | Our results demonstrate an imbalance of RANKL/OPG expression associated with diabetes that may contribute to the delay of fracture repair during the course of diabetes. |
| 216 | 18592139 | Imbalance of RANK, RANKL and OPG expression during tibial fracture repair in diabetic rats. |
| 217 | 18592139 | To clarify the mechanisms of altered bone repair in the diabetic state, we investigated RANK, RANKL and OPG expression by immunohistochemistry and RT-PCR in the fracture sites of rats that were either healthy or made diabetic by alloxan. |
| 218 | 18592139 | The number of RANK, RANKL and OPG positive cells was decreased in the db group; however, the RANKL/OPG ratio was similar in controls and db at this time. |
| 219 | 18592139 | At day 14, numbers of RANKL and OPG positive cells and the mRNA expression for these markers were higher in the control group than in db (P = 0.008). |
| 220 | 18592139 | The RANKL/OPG ratio in the db group was greater than in controls. |
| 221 | 18592139 | Our results demonstrate an imbalance of RANKL/OPG expression associated with diabetes that may contribute to the delay of fracture repair during the course of diabetes. |
| 222 | 18599037 | Compared with control incubation, 2-deoxy-d-ribose significantly (P<0.05) inhibited alkaline phosphatase (ALP) activity, collagen content, and calcium deposition at the concentration of 20 mM. |
| 223 | 18599037 | Myricetin significantly (P<0.05) increased cell survival, ALP activity, collagen, osteocalcin, osteoprotegerin, and calcium deposition and decreased MDA, protein carbonyl, and advanced oxidation protein products contents of osteoblastic MC3T3-E1 cells in the presence of 20 mM 2-deoxy-d-ribose. |
| 224 | 18716364 | We measured blood counts, blood chemistry, bone alkaline phosphatase, intact-PTH, interleukin-6, osteoprotegerin (OPG), hemoglobin A1c, 25-hydroxyvitamin D (25(OH)D) and fetuin-A. |
| 225 | 18716364 | Multiple regression analyses showed that low albumin and high OPG were associated with high CACS. |
| 226 | 18716364 | Serum OPG was positively associated with high CACS and can be a useful screening tool for severe coronary calcification, whereas no association between fetuin-A and CACS was found. |
| 227 | 18716364 | We measured blood counts, blood chemistry, bone alkaline phosphatase, intact-PTH, interleukin-6, osteoprotegerin (OPG), hemoglobin A1c, 25-hydroxyvitamin D (25(OH)D) and fetuin-A. |
| 228 | 18716364 | Multiple regression analyses showed that low albumin and high OPG were associated with high CACS. |
| 229 | 18716364 | Serum OPG was positively associated with high CACS and can be a useful screening tool for severe coronary calcification, whereas no association between fetuin-A and CACS was found. |
| 230 | 18716364 | We measured blood counts, blood chemistry, bone alkaline phosphatase, intact-PTH, interleukin-6, osteoprotegerin (OPG), hemoglobin A1c, 25-hydroxyvitamin D (25(OH)D) and fetuin-A. |
| 231 | 18716364 | Multiple regression analyses showed that low albumin and high OPG were associated with high CACS. |
| 232 | 18716364 | Serum OPG was positively associated with high CACS and can be a useful screening tool for severe coronary calcification, whereas no association between fetuin-A and CACS was found. |
| 233 | 18789716 | Relationship of elevated osteoprotegerin with insulin resistance, CRP, and TNF-alpha levels in men with type 2 diabetes. |
| 234 | 19083628 | In the pathogenesis of Charcot neuroarthropathy, recent advances in our understanding of the mechanisms underlying the development of osteopenia and osteoporosis include the central role of the RANK-L OPG signalling system. |
| 235 | 19196804 | Role of parathyroid hormone-related protein in the decreased osteoblast function in diabetes-related osteopenia. |
| 236 | 19196804 | We examined here whether diabetes-associated changes in osteoblast phenotype might in part result from a decrease in PTH-related protein (PTHrP). |
| 237 | 19196804 | These skeletal alterations were associated with decreased gene expression (by real-time PCR) of Runx2, osterix, osteocalcin, PTHrP, the PTH type 1 receptor, vascular endothelial growth factor and its receptors, and osteoprotegerin to receptor activator of nuclear factor-kappaB ligand mRNA ratio, and increased peroxisome proliferator-activated receptor-gamma2 mRNA levels. |
| 238 | 19219381 | Effect of GLP-1 treatment on bone turnover in normal, type 2 diabetic, and insulin-resistant states. |
| 239 | 19219381 | Since GLP-1 is decreased in the latter condition, we evaluated some bone characteristics in streptozotocin-induced type 2 diabetic (T2D) and fructose-induced insulin-resistant (IR) rat models compared to normal (N) and the effect of GLP-1 or saline (control) treatment (3 days by osmotic pump). |
| 240 | 19219381 | Compared to N, plasma glucose and insulin were, respectively, higher and lower in T2D; osteocalcin (OC) and tartrate-resistant alkaline phosphatase 5b were lower; phosphate in IR showed a tendency to be higher; PTH was not different in T2D and IR; all parameters were unchanged after GLP-1 infusion. |
| 241 | 19219381 | Bone OC, osteoprotegerin (OPG) and RANKL mRNA were lower in T2D and IR; GLP-1 increased OC and OPG in all groups and RANKL in T2D. |
| 242 | 19219381 | These findings show an insulin-independent anabolic effect of GLP-1 and suggest that GLP-1 could be a useful therapeutic agent for improving the deficient bone formation and bone structure associated with glucose intolerance. |
| 243 | 19240767 | TNF-related apoptosisinducing ligand (TRAIL) and osteoprotegerin had the highest level of expression. |
| 244 | 19240767 | Inflammatory cytokines, including MIF via CD74, upregulate TRAIL. |
| 245 | 19388970 | Association between plasma osteoprotegerin concentrations and urinary albumin excretion in Type 2 diabetes. |
| 246 | 19415676 | An intracellular role of the S100 family member S100A4 (Mts1) to suppress mineralization has been described in pre-osteoblastic MC3T3-E1 cells. |
| 247 | 19415676 | RANKL-treated RAW 264.7 cell proliferation and TRAP activity were significantly inhibited by S100, and the number and size of TRAP-positive multinucleated cells were decreased. |
| 248 | 19415676 | In contrast to the direct inhibitory effect of S100, the conditioned media promoted RAW 264.7 cell proliferation and TRAP activity, with a trend toward increased TRAP-positive multinucleated cells. |
| 249 | 19415676 | S100 treatment of the MC3T3-E1 cells for 14 days did not significantly affect alkaline phosphatase, M-CSF, or OPG gene expression. |
| 250 | 19495918 | However, high-dose STZ caused a more rapid elevation of blood glucose levels and a greater magnitude of change in body mass, fat pad mass, and bone gene expression (osteocalcin, aP2). |
| 251 | 19495918 | An increase in cathepsin K and in the ratio of RANKL/OPG was noted in high-dose STZ mice, suggesting the possibility that severe diabetes could increase osteoclast activity, something not seen with lower doses. |
| 252 | 19497632 | Plasma bone-related peptides osteopontin and osteoprotegerin levels were measured. |
| 253 | 19497632 | In diabetic patients classified into tertiles according to their CACS levels, those with the highest scores showed the highest mean-IMT (p=0.0004) and bone-related peptides (p<0.05) among the groups. log(CACS+1) and mean-IMT were associated (p<0.0001) and were positively correlated with osteopontin (p<0.01) and osteoprotegerin (p<0.01) in diabetic patients. |
| 254 | 19497632 | Multivariate analyses revealed that the significant independent determinants of log(CACS+1) were age, duration of diabetes and osteopontin (p<0.0001) and those of mean-IMT were age, hypertension, osteopontin and osteoprotegerin (p<0.0001), respectively. |
| 255 | 19497632 | Plasma bone-related peptides osteopontin and osteoprotegerin levels were measured. |
| 256 | 19497632 | In diabetic patients classified into tertiles according to their CACS levels, those with the highest scores showed the highest mean-IMT (p=0.0004) and bone-related peptides (p<0.05) among the groups. log(CACS+1) and mean-IMT were associated (p<0.0001) and were positively correlated with osteopontin (p<0.01) and osteoprotegerin (p<0.01) in diabetic patients. |
| 257 | 19497632 | Multivariate analyses revealed that the significant independent determinants of log(CACS+1) were age, duration of diabetes and osteopontin (p<0.0001) and those of mean-IMT were age, hypertension, osteopontin and osteoprotegerin (p<0.0001), respectively. |
| 258 | 19497632 | Plasma bone-related peptides osteopontin and osteoprotegerin levels were measured. |
| 259 | 19497632 | In diabetic patients classified into tertiles according to their CACS levels, those with the highest scores showed the highest mean-IMT (p=0.0004) and bone-related peptides (p<0.05) among the groups. log(CACS+1) and mean-IMT were associated (p<0.0001) and were positively correlated with osteopontin (p<0.01) and osteoprotegerin (p<0.01) in diabetic patients. |
| 260 | 19497632 | Multivariate analyses revealed that the significant independent determinants of log(CACS+1) were age, duration of diabetes and osteopontin (p<0.0001) and those of mean-IMT were age, hypertension, osteopontin and osteoprotegerin (p<0.0001), respectively. |
| 261 | 19586609 | Blood was taken before and after treatment for plasma measurements; tibiae and femurs were collected for gene expression of bone markers (RT-PCR) and structure (microCT) analysis; we also measured the mRNA levels of LRP5 - an activator of the Wnt pathway - and those of DKK1 and sclerostin (SOST) - both blockers of LRP5 activity. |
| 262 | 19586609 | Compared to N-control, plasma glucose and insulin were respectively higher and lower in T2D; osteocalcin (OC) and tartrate-resistant alkaline phosphatase 5b (TRAP5b) were lower; after Ex-4, these turnover markers were further reduced in T2D and IR, while TRAP5b increased in N. |
| 263 | 19586609 | Bone OC, osteoprogeterin (OPG) and receptor activator of NF-kB ligand (RANKL) mRNA were lower in T2D and IR; Ex-4 increased OC in all groups and OPG in N and IR, reduced RANKL in N and T2D but increased it in IR; the LRP5/DKK1 and LRP5/SOST mRNA ratios were similarly decreased in T2D, but in IR, the latter ratio was reduced while the former was increased; after Ex-4, both ratios augmented in N, and that of LRP5/DKK1 tended to normalize in T2D and IR. |
| 264 | 19816015 | Calcium-phosphate product (Ca x P), body mass index (BMI), fetuin-A, osteoprotegerin (OPG), osteopontin, transforming growth factor-beta1 (TGF-beta1), fibroblast growth factor-23 (FGF-23) and matrix Gla protein (MGP) were considered. |
| 265 | 19816015 | Multivariate regression analysis, adjusted for age and for dialysis vintage, showed that TGF-beta1, OPG and days with Ca x P >55 mg/dl are independent predictors of CAC, while MGP was shown to be a protective factor. |
| 266 | 19816015 | Calcium-phosphate product (Ca x P), body mass index (BMI), fetuin-A, osteoprotegerin (OPG), osteopontin, transforming growth factor-beta1 (TGF-beta1), fibroblast growth factor-23 (FGF-23) and matrix Gla protein (MGP) were considered. |
| 267 | 19816015 | Multivariate regression analysis, adjusted for age and for dialysis vintage, showed that TGF-beta1, OPG and days with Ca x P >55 mg/dl are independent predictors of CAC, while MGP was shown to be a protective factor. |
| 268 | 19922962 | Cardiovascular risk factors, high-sensitivity C-reactive protein, and OPG were measured. |
| 269 | 19922962 | In multiple logistic regression analysis, type 2 diabetes mellitus showed a significant association with serum OPG levels when adjustments were made for age, high-sensitivity C-reactive protein, and cardiovascular risk factors (odds ratio = 2.21; confidence interval, 1.34-3.66; P = .002). |
| 270 | 19922962 | Cardiovascular risk factors, high-sensitivity C-reactive protein, and OPG were measured. |
| 271 | 19922962 | In multiple logistic regression analysis, type 2 diabetes mellitus showed a significant association with serum OPG levels when adjustments were made for age, high-sensitivity C-reactive protein, and cardiovascular risk factors (odds ratio = 2.21; confidence interval, 1.34-3.66; P = .002). |
| 272 | 19924377 | MSC cultured in osteogenic medium increased expression of osteonectin, Runt-related transcription factor 2 (RUNX-2), osteocalcin, and alkaline phosphatase. |
| 273 | 19924377 | Additionally, the effect of HO-1 on osteoblasts appears different to that seen in adipocyte stem cells. |
| 274 | 19924377 | Moreover, glucose (30 mM) inhibited osteoblast differentiation, as evidenced by decreased bone morphogenetic protein (BMP)-2, osteonectin, osteocalcin, and osteoprotegerin (OPG). |
| 275 | 19924377 | Increased HO-1 expression increased the levels of osteonectin, OPG, and BMP-2. |
| 276 | 19924377 | Inhibition of HO activity prevented the increase in osteonectin and potentiated the decrease of osteocalcin and OPG in cells exposed to high glucose levels. |
| 277 | 19924377 | Furthermore, targeting HO-1 expression increased pAMPK and endothelial nitric oxide synthase (eNOS) and restored osteoblastic markers. |
| 278 | 19924377 | MSC cultured in osteogenic medium increased expression of osteonectin, Runt-related transcription factor 2 (RUNX-2), osteocalcin, and alkaline phosphatase. |
| 279 | 19924377 | Additionally, the effect of HO-1 on osteoblasts appears different to that seen in adipocyte stem cells. |
| 280 | 19924377 | Moreover, glucose (30 mM) inhibited osteoblast differentiation, as evidenced by decreased bone morphogenetic protein (BMP)-2, osteonectin, osteocalcin, and osteoprotegerin (OPG). |
| 281 | 19924377 | Increased HO-1 expression increased the levels of osteonectin, OPG, and BMP-2. |
| 282 | 19924377 | Inhibition of HO activity prevented the increase in osteonectin and potentiated the decrease of osteocalcin and OPG in cells exposed to high glucose levels. |
| 283 | 19924377 | Furthermore, targeting HO-1 expression increased pAMPK and endothelial nitric oxide synthase (eNOS) and restored osteoblastic markers. |
| 284 | 19924377 | MSC cultured in osteogenic medium increased expression of osteonectin, Runt-related transcription factor 2 (RUNX-2), osteocalcin, and alkaline phosphatase. |
| 285 | 19924377 | Additionally, the effect of HO-1 on osteoblasts appears different to that seen in adipocyte stem cells. |
| 286 | 19924377 | Moreover, glucose (30 mM) inhibited osteoblast differentiation, as evidenced by decreased bone morphogenetic protein (BMP)-2, osteonectin, osteocalcin, and osteoprotegerin (OPG). |
| 287 | 19924377 | Increased HO-1 expression increased the levels of osteonectin, OPG, and BMP-2. |
| 288 | 19924377 | Inhibition of HO activity prevented the increase in osteonectin and potentiated the decrease of osteocalcin and OPG in cells exposed to high glucose levels. |
| 289 | 19924377 | Furthermore, targeting HO-1 expression increased pAMPK and endothelial nitric oxide synthase (eNOS) and restored osteoblastic markers. |
| 290 | 20098449 | In addition, two components of the TNF superfamily, namely TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) and osteoprotegerin, may be involved in the pathogenesis of diabetic angiopathy. |
| 291 | 20146170 | Recently, two single nucleotide polymorphisms, rs4355801 near the osteoprotegerin (OPG) gene and rs3736228 in the low-density lipoprotein receptor-related protein 5 (LRP5) gene, were found to be associated with osteoporosis and osteoporotic fractures in Caucasians in a genome wide association study. |
| 292 | 20192865 | Salivary interleukin-6, matrix metalloproteinase-8, and osteoprotegerin in patients with periodontitis and diabetes. |
| 293 | 20354684 | In previous studies, with up to 16 weeks of exposure to rosiglitazone or pioglitazone, circulating markers of bone formation [procollagen I N-terminal propeptide (P1NP), osteocalcin, and bone-specific alkaline phosphatase] decreased but no change in bone resorption markers was found. |
| 294 | 20354684 | Overall, in stratified analyses of men and in stratified analyses among different ethnicities, there were no statistically significant differences observed in CTX, P1NP, OPG, PTH, or 25-OHD between the treatment groups. |
| 295 | 20476881 | Receptor activator of nuclear factor-kappa B ligand/osteoprotegerin ratio in sites of chronic periodontitis of subjects with poorly and well-controlled type 2 diabetes. |
| 296 | 20570543 | In particular, new data have emerged on the central role of the RANK/RANK-ligand (RANK-L)/osteoprotegerin (OPG) system in the pathogenesis of osteopenia. |
| 297 | 20570543 | As the cornerstone of treatment remains any method that avoids weight-bearing on the foot, the primary importance of the RANK/RANK-L/OPG signalling pathway is that it opens up the field to new treatment strategies for the future. |
| 298 | 20703212 | The expression of TNF-related apoptosis-inducing ligand (TRAIL), its decoy receptor osteoprotegerin, and receptors Fas (a Fas ligand receptor) and CD74 (a migration inhibitory factor (MIF) receptor) were induced in human diabetic nephropathy. |
| 299 | 20716128 | Arterial calcification is the result of a complex interplay between stimulating (bone morphogenetic protein type 2 [BMP-2], RANKL) and inhibitory (matrix Gla protein, BMP-7, osteoprotegerin, fetuin-A, osteopontin) proteins. |
| 300 | 20818503 | Increased expression of the receptor for activation of NF-kappaB and decreased runt-related transcription factor 2 expression in bone of rats with streptozotocin-induced diabetes. |
| 301 | 20818503 | Insulin-dependent diabetes mellitus (IDDM) is associated with an increased risk of osteopenia/osteoporosis in humans. |
| 302 | 20818503 | Markers of bone formation, alkaline phosphatase (ALP) activity and the number of osteoblasts in the proximal tibia and the serum osteocalcin level, were significantly lower. |
| 303 | 20818503 | Markers of bone resorption, activity of tartrate-resistant acid phosphatase (TRAP) and cathepsin K and the number of osteoclasts in the proximal tibia and urinary excretion of deoxypyridinoline, were higher in diabetic rats than control rats. mRNA levels of receptor for activation of NF-kappaB (RANK), c-fos, c-jun, TRAP and cathepsin K were significantly increased in diabetic rats, although RANK ligand, osteoprotegerin, macrophage colony-stimulating factor and c-fms levels were similar to the control value. |
| 304 | 20818503 | The decreased expression of ALP, osteoclacin and collagen mRNA in diabetic rats was associated with decreases in the expression of Runx2, Dlx5 and osterix and an unaltered expression of bone morphogenic protein-2. |
| 305 | 20818503 | The level of RANK protein increased and Runx2 protein decreased in diabetic rats. |
| 306 | 20818503 | These suggested that short-term IDDM induced upregulation of osteoclastogenesis with an increase in RANK and downregulation of osteoblastogenesis with a decrease in Runx2 in bone. |
| 307 | 20953353 | Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury. |
| 308 | 20953353 | TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy. |
| 309 | 20953353 | TRAIL activates NF-kappaB in tubular cells and promotes apoptosis in tubular cells and podocytes, especially in a high-glucose environment. |
| 310 | 20953353 | By contrast, osteoprotegerin plays a protective role against TRAIL-induced apoptosis. |
| 311 | 20953353 | Another family member, TNF-like weak inducer of apoptosis (TWEAK induces inflammation and tubular cell death or proliferation, depending on the microenvironment. |
| 312 | 20953353 | While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses. |
| 313 | 20953353 | TWEAK promotes the secretion of MCP-1 and RANTES through NF-kappaB RelA-containing complexes and upregulates CCl21 and CCL19 expression through NF-kappaB inducing kinase (NIK-) dependent RelB/NF-kappaB2 complexes. |
| 314 | 20953353 | Tumor necrosis factor (TNF) and Fas ligand regulate renal cell survival and inflammation, and therapeutic targeting improves the outcome of experimental renal injury. |
| 315 | 20953353 | TNF-related apoptosis-inducing ligand (TRAIL and its potential decoy receptor osteoprotegerin are the two most upregulated death-related genes in human diabetic nephropathy. |
| 316 | 20953353 | TRAIL activates NF-kappaB in tubular cells and promotes apoptosis in tubular cells and podocytes, especially in a high-glucose environment. |
| 317 | 20953353 | By contrast, osteoprotegerin plays a protective role against TRAIL-induced apoptosis. |
| 318 | 20953353 | Another family member, TNF-like weak inducer of apoptosis (TWEAK induces inflammation and tubular cell death or proliferation, depending on the microenvironment. |
| 319 | 20953353 | While TNF only activates canonical NF-kappaB signaling, TWEAK promotes both canonical and noncanonical NF-kappaB activation in tubular cells, regulating different inflammatory responses. |
| 320 | 20953353 | TWEAK promotes the secretion of MCP-1 and RANTES through NF-kappaB RelA-containing complexes and upregulates CCl21 and CCL19 expression through NF-kappaB inducing kinase (NIK-) dependent RelB/NF-kappaB2 complexes. |
| 321 | 20970873 | Fasting glucose, insulin, serum lipids, CRP and OPG were assayed. |
| 322 | 20970873 | Serum OPG levels were associated with obesity, insulin resistance, serum CRP and carotid IMT. |
| 323 | 20970873 | Fasting glucose, insulin, serum lipids, CRP and OPG were assayed. |
| 324 | 20970873 | Serum OPG levels were associated with obesity, insulin resistance, serum CRP and carotid IMT. |
| 325 | 21251686 | Serum osteoprotegerin and tumor necrosis factor related apoptosis inducing-ligand (TRAIL) are elevated in type 2 diabetic patients with albuminuria and serum osteoprotegerin is independently associated with the severity of diabetic nephropathy. |
| 326 | 21251686 | Osteoprotegerin (OPG) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) have recently been reported to be associated with diabetic nephropathy in an in vitro study. |
| 327 | 21251686 | However, the literature regarding serum OPG and TRAIL in type 2 diabetes mellitus patients is scarce. |
| 328 | 21251686 | To investigate the role of OPG/TRAIL in diabetic nephropathy, we measured the serum concentrations of OPG and TRAIL in type 2 diabetes mellitus patients with different stages of nephropathy by enzyme-linked immunosorbent assay. |
| 329 | 21251686 | The serum concentrations of OPG and TRAIL were significantly elevated in patients with microalbuminuria (OPG, 2154.2 ± 922.1 pg/mL; TRAIL, 80.2 ± 24.1 pg/mL) and macroalbuminuria (OPG, 2251.5 ± 925.7 pg/mL; TRAIL, 88.1 ± 23.8 pg/mL) as compared with patients with normoalbuminuria (OPG, 1690.1 ± 627.2 pg/mL; TRAIL, 70.7 ± 23.3 pg/mL). |
| 330 | 21251686 | Serum OPG and TRAIL levels were increased in parallel and were significantly associated with each other. |
| 331 | 21251686 | Serum osteoprotegerin and tumor necrosis factor related apoptosis inducing-ligand (TRAIL) are elevated in type 2 diabetic patients with albuminuria and serum osteoprotegerin is independently associated with the severity of diabetic nephropathy. |
| 332 | 21251686 | Osteoprotegerin (OPG) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) have recently been reported to be associated with diabetic nephropathy in an in vitro study. |
| 333 | 21251686 | However, the literature regarding serum OPG and TRAIL in type 2 diabetes mellitus patients is scarce. |
| 334 | 21251686 | To investigate the role of OPG/TRAIL in diabetic nephropathy, we measured the serum concentrations of OPG and TRAIL in type 2 diabetes mellitus patients with different stages of nephropathy by enzyme-linked immunosorbent assay. |
| 335 | 21251686 | The serum concentrations of OPG and TRAIL were significantly elevated in patients with microalbuminuria (OPG, 2154.2 ± 922.1 pg/mL; TRAIL, 80.2 ± 24.1 pg/mL) and macroalbuminuria (OPG, 2251.5 ± 925.7 pg/mL; TRAIL, 88.1 ± 23.8 pg/mL) as compared with patients with normoalbuminuria (OPG, 1690.1 ± 627.2 pg/mL; TRAIL, 70.7 ± 23.3 pg/mL). |
| 336 | 21251686 | Serum OPG and TRAIL levels were increased in parallel and were significantly associated with each other. |
| 337 | 21251686 | Serum osteoprotegerin and tumor necrosis factor related apoptosis inducing-ligand (TRAIL) are elevated in type 2 diabetic patients with albuminuria and serum osteoprotegerin is independently associated with the severity of diabetic nephropathy. |
| 338 | 21251686 | Osteoprotegerin (OPG) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) have recently been reported to be associated with diabetic nephropathy in an in vitro study. |
| 339 | 21251686 | However, the literature regarding serum OPG and TRAIL in type 2 diabetes mellitus patients is scarce. |
| 340 | 21251686 | To investigate the role of OPG/TRAIL in diabetic nephropathy, we measured the serum concentrations of OPG and TRAIL in type 2 diabetes mellitus patients with different stages of nephropathy by enzyme-linked immunosorbent assay. |
| 341 | 21251686 | The serum concentrations of OPG and TRAIL were significantly elevated in patients with microalbuminuria (OPG, 2154.2 ± 922.1 pg/mL; TRAIL, 80.2 ± 24.1 pg/mL) and macroalbuminuria (OPG, 2251.5 ± 925.7 pg/mL; TRAIL, 88.1 ± 23.8 pg/mL) as compared with patients with normoalbuminuria (OPG, 1690.1 ± 627.2 pg/mL; TRAIL, 70.7 ± 23.3 pg/mL). |
| 342 | 21251686 | Serum OPG and TRAIL levels were increased in parallel and were significantly associated with each other. |
| 343 | 21251686 | Serum osteoprotegerin and tumor necrosis factor related apoptosis inducing-ligand (TRAIL) are elevated in type 2 diabetic patients with albuminuria and serum osteoprotegerin is independently associated with the severity of diabetic nephropathy. |
| 344 | 21251686 | Osteoprotegerin (OPG) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) have recently been reported to be associated with diabetic nephropathy in an in vitro study. |
| 345 | 21251686 | However, the literature regarding serum OPG and TRAIL in type 2 diabetes mellitus patients is scarce. |
| 346 | 21251686 | To investigate the role of OPG/TRAIL in diabetic nephropathy, we measured the serum concentrations of OPG and TRAIL in type 2 diabetes mellitus patients with different stages of nephropathy by enzyme-linked immunosorbent assay. |
| 347 | 21251686 | The serum concentrations of OPG and TRAIL were significantly elevated in patients with microalbuminuria (OPG, 2154.2 ± 922.1 pg/mL; TRAIL, 80.2 ± 24.1 pg/mL) and macroalbuminuria (OPG, 2251.5 ± 925.7 pg/mL; TRAIL, 88.1 ± 23.8 pg/mL) as compared with patients with normoalbuminuria (OPG, 1690.1 ± 627.2 pg/mL; TRAIL, 70.7 ± 23.3 pg/mL). |
| 348 | 21251686 | Serum OPG and TRAIL levels were increased in parallel and were significantly associated with each other. |
| 349 | 21251686 | Serum osteoprotegerin and tumor necrosis factor related apoptosis inducing-ligand (TRAIL) are elevated in type 2 diabetic patients with albuminuria and serum osteoprotegerin is independently associated with the severity of diabetic nephropathy. |
| 350 | 21251686 | Osteoprotegerin (OPG) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) have recently been reported to be associated with diabetic nephropathy in an in vitro study. |
| 351 | 21251686 | However, the literature regarding serum OPG and TRAIL in type 2 diabetes mellitus patients is scarce. |
| 352 | 21251686 | To investigate the role of OPG/TRAIL in diabetic nephropathy, we measured the serum concentrations of OPG and TRAIL in type 2 diabetes mellitus patients with different stages of nephropathy by enzyme-linked immunosorbent assay. |
| 353 | 21251686 | The serum concentrations of OPG and TRAIL were significantly elevated in patients with microalbuminuria (OPG, 2154.2 ± 922.1 pg/mL; TRAIL, 80.2 ± 24.1 pg/mL) and macroalbuminuria (OPG, 2251.5 ± 925.7 pg/mL; TRAIL, 88.1 ± 23.8 pg/mL) as compared with patients with normoalbuminuria (OPG, 1690.1 ± 627.2 pg/mL; TRAIL, 70.7 ± 23.3 pg/mL). |
| 354 | 21251686 | Serum OPG and TRAIL levels were increased in parallel and were significantly associated with each other. |
| 355 | 21251686 | Serum osteoprotegerin and tumor necrosis factor related apoptosis inducing-ligand (TRAIL) are elevated in type 2 diabetic patients with albuminuria and serum osteoprotegerin is independently associated with the severity of diabetic nephropathy. |
| 356 | 21251686 | Osteoprotegerin (OPG) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) have recently been reported to be associated with diabetic nephropathy in an in vitro study. |
| 357 | 21251686 | However, the literature regarding serum OPG and TRAIL in type 2 diabetes mellitus patients is scarce. |
| 358 | 21251686 | To investigate the role of OPG/TRAIL in diabetic nephropathy, we measured the serum concentrations of OPG and TRAIL in type 2 diabetes mellitus patients with different stages of nephropathy by enzyme-linked immunosorbent assay. |
| 359 | 21251686 | The serum concentrations of OPG and TRAIL were significantly elevated in patients with microalbuminuria (OPG, 2154.2 ± 922.1 pg/mL; TRAIL, 80.2 ± 24.1 pg/mL) and macroalbuminuria (OPG, 2251.5 ± 925.7 pg/mL; TRAIL, 88.1 ± 23.8 pg/mL) as compared with patients with normoalbuminuria (OPG, 1690.1 ± 627.2 pg/mL; TRAIL, 70.7 ± 23.3 pg/mL). |
| 360 | 21251686 | Serum OPG and TRAIL levels were increased in parallel and were significantly associated with each other. |
| 361 | 21464945 | Prominent bone loss mediated by RANKL and IL-17 produced by CD4+ T cells in TallyHo/JngJ mice. |
| 362 | 21464945 | The osteoblast-specific bone forming markers osteocalcin and osteoprotegerin were decreased in TH mice, whereas osteoclast-driven bone resorption markers such as IL-6 and RANKL were significantly elevated in the bone marrow and blood of TH mice. |
| 363 | 21464945 | In addition, RANKL expression was prominently increased in CD4+ T cells of TH mice upon T cell receptor stimulation, which was in accordance with enhanced IL-17 production. |
| 364 | 21464945 | IL-17 production in CD4+ T cells was directly promoted by treatment with leptin while IFN-γ production was not. |
| 365 | 21464945 | These results strongly indicate that increased leptin in TH mice may act in conjunction with IL-6 to preferentially stimulate IL-17 production in CD4+ T cells and induce RANKL-mediated osteoclastogenesis. |
| 366 | 21659498 | The RANKL/RANK/OPG signaling pathway mediates medial arterial calcification in diabetic Charcot neuroarthropathy. |
| 367 | 21823052 | The purpose of this study was to explore whether mechanical loading by exercise over a 1-year period in postmenopausal women had an effect on the receptor activator for nuclear factor kappa B ligand/osteoprotegerin (RANKL/OPG) system or the levels of the Wnt-signaling antagonist sclerostin. |
| 368 | 21823052 | Blood samples were taken from participants at baseline and after 1 year and serum levels of OPG, RANKL and sclerostin were quantified together with the bone metabolism markers C-terminal telopeptide of collagen type I (CTX) and bone-specific alkaline phosphatase (BALP). |
| 369 | 21823052 | Although our study is limited in number of participating women, we have been able to show an OPG-associated, and RANKL- and sclerostin-independent, training-induced inhibition of postmenopausal bone loss. |
| 370 | 21823052 | The purpose of this study was to explore whether mechanical loading by exercise over a 1-year period in postmenopausal women had an effect on the receptor activator for nuclear factor kappa B ligand/osteoprotegerin (RANKL/OPG) system or the levels of the Wnt-signaling antagonist sclerostin. |
| 371 | 21823052 | Blood samples were taken from participants at baseline and after 1 year and serum levels of OPG, RANKL and sclerostin were quantified together with the bone metabolism markers C-terminal telopeptide of collagen type I (CTX) and bone-specific alkaline phosphatase (BALP). |
| 372 | 21823052 | Although our study is limited in number of participating women, we have been able to show an OPG-associated, and RANKL- and sclerostin-independent, training-induced inhibition of postmenopausal bone loss. |
| 373 | 22238287 | Moreover, plasma phosphorus concentration, calcium × phosphorus product and alkaline phosphatase (ALP) activity, and aortic calcium content and ALP activity were significantly increased. |
| 374 | 22238287 | Fructose feeding increased mRNA levels of osteopontin, type III sodium-dependent phosphate co-transporter, bone morphogenetic protein-2 and the key transcription factor core binding factor alpha 1 in aortic tissue and downregulated mRNA levels of osteoprotegerin and matrix γ-carboxyglutamic acid protein. |
| 375 | 22278426 | Serum osteoprotegerin, RANKL, and Dkk-1 levels in adults with Langerhans cell histiocytosis. |
| 376 | 22301390 | The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. |
| 377 | 22301390 | RANKL and OPG mRNA levels, protein content, and location were determined. |
| 378 | 22301390 | PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. |
| 379 | 22301390 | DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. |
| 380 | 22301390 | The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. |
| 381 | 22301390 | RANKL and OPG mRNA levels, protein content, and location were determined. |
| 382 | 22301390 | PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. |
| 383 | 22301390 | DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. |
| 384 | 22301390 | The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. |
| 385 | 22301390 | RANKL and OPG mRNA levels, protein content, and location were determined. |
| 386 | 22301390 | PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. |
| 387 | 22301390 | DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. |
| 388 | 22301390 | The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. |
| 389 | 22301390 | RANKL and OPG mRNA levels, protein content, and location were determined. |
| 390 | 22301390 | PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. |
| 391 | 22301390 | DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. |
| 392 | 22496403 | Osteoprotegerin, leptin and IL-6: association with silent myocardial ischemia in type 2 diabetes mellitus. |
| 393 | 22699799 | LED irradiation also inhibited the osteoclastogenesis in MC3T3-E1 cells by regulating the receptor activator of nuclear factor kappa-B ligand and osteoprotegerin. |
| 394 | 22752126 | In a population-based study, cardiovascular risk factors, high-sensitivity C-reactive protein (hs-CRP), osteoprotegerin, receptor activator of nuclear factor-κB ligand, osteocalcin, CrossLaps, alkaline phosphatase, and bone mineral density (BMD) at the lumbar spine (L2-L4) and the proximal femur were measured in 382 Iranian postmenopausal women. |
| 395 | 22752126 | Since CrossLaps and alkaline phosphatase levels were independently associated with the presence of type 2 diabetes mellitus, the unique contribution of osteocalcin in glucose metabolism could not be concluded. |
| 396 | 22803952 | The effect of exercise on osteoprotegerin and TNF-related apoptosis-inducing ligand in obese patients. |
| 397 | 22841521 | A comparison of osteoprotegerin with adiponectin and high-sensitivity C-reactive protein (hsCRP) as a marker for insulin resistance. |
| 398 | 22965192 | Osteoprotegerin (OPG) is a secretory glycoprotein that belongs to the tumor necrosis factor receptor family and plays a role in atherosclerosis. |
| 399 | 23023373 | Multimarker risk assessment including osteoprotegerin and CXCL16 in acute coronary syndromes. |
| 400 | 23052229 | Results showed that SM22α-Rankl ( tg ) SMCs had higher baseline alkaline phosphatase (ALP) activity but not baseline matrix calcification. |
| 401 | 23052229 | Real-time RT-qPCR revealed higher baseline expression of ALP and ankylosis genes but lower osteoprotegerin gene in SM22α-Rankl ( tg ) SMCs. |
| 402 | 23128413 | In addition, treatment with glabridin resulted in a significant elevation of alkaline phosphatase (ALP) activity, collagen contents and osteoblast differentiation genes [ALP, collagen, osteopontin (OPN), osteoprotegerin (OPG) and osteocalcin (OC)] and bone morphogenetic protein (BMP) genes (BMP2, BMP4 and BMP7). |
| 403 | 23128413 | Glabridin also upregulated the gene expression of antioxidant enzymes, superoxide dismutase 1 (SOD1) and glutathione peroxidase 4 (GPX4), which were inhibited by dRib. |
| 404 | 23178165 | Amylin failed to affect glycaemia or parathyroid hormone levels in any group, but reduced hyperinsulinemia in IR rats. |
| 405 | 23178165 | In contrast, in IR rats, no apparent osteogenic effect of amylin in the femur was observed, although both OC and OPG/RANKL ratio were increased in the tibia. |
| 406 | 23219833 | Mutations in K-Ras linked to levels of osteoprotegerin and sensitivity to TRAIL-induced cell death in pancreatic ductal adenocarcinoma cells. |
| 407 | 23219833 | Pancreatic ductal adenocarcinoma (PDAC) cell lines were found to secrete OPG and the level of OPG production correlated with sensitivity to TRAIL-induced apoptosis. |
| 408 | 23219833 | Silencing OPG sensitized cells to TRAIL-induced apoptosis. |
| 409 | 23219833 | Interestingly, a positive correlation was noted between OPG production level and K-Ras mutation status. |
| 410 | 23219833 | Earlier studies implicated K-Ras in conferring resistance to TRAIL-induced apoptosis in pancreatic cells and this study demonstrates that K-Ras mediated TRAIL resistance in pancreatic cancer cells occurs due to increased OPG production. |
| 411 | 23219833 | Silencing K-Ras in pancreatic cancer cells decreased OPG levels and increased sensitivity to TRAIL-induced apoptosis. |
| 412 | 23219833 | These observations indicate that OPG can play a role in both cell survival and in PDAC cell sensitivity to TRAIL-induced apoptosis, which may contribute to metastasis. |
| 413 | 23219833 | Targeted inhibition of OPG binding to TRAIL may represent a therapeutic approach in the treatment of pancreatic cancer. |
| 414 | 23219833 | Mutations in K-Ras linked to levels of osteoprotegerin and sensitivity to TRAIL-induced cell death in pancreatic ductal adenocarcinoma cells. |
| 415 | 23219833 | Pancreatic ductal adenocarcinoma (PDAC) cell lines were found to secrete OPG and the level of OPG production correlated with sensitivity to TRAIL-induced apoptosis. |
| 416 | 23219833 | Silencing OPG sensitized cells to TRAIL-induced apoptosis. |
| 417 | 23219833 | Interestingly, a positive correlation was noted between OPG production level and K-Ras mutation status. |
| 418 | 23219833 | Earlier studies implicated K-Ras in conferring resistance to TRAIL-induced apoptosis in pancreatic cells and this study demonstrates that K-Ras mediated TRAIL resistance in pancreatic cancer cells occurs due to increased OPG production. |
| 419 | 23219833 | Silencing K-Ras in pancreatic cancer cells decreased OPG levels and increased sensitivity to TRAIL-induced apoptosis. |
| 420 | 23219833 | These observations indicate that OPG can play a role in both cell survival and in PDAC cell sensitivity to TRAIL-induced apoptosis, which may contribute to metastasis. |
| 421 | 23219833 | Targeted inhibition of OPG binding to TRAIL may represent a therapeutic approach in the treatment of pancreatic cancer. |
| 422 | 23219833 | Mutations in K-Ras linked to levels of osteoprotegerin and sensitivity to TRAIL-induced cell death in pancreatic ductal adenocarcinoma cells. |
| 423 | 23219833 | Pancreatic ductal adenocarcinoma (PDAC) cell lines were found to secrete OPG and the level of OPG production correlated with sensitivity to TRAIL-induced apoptosis. |
| 424 | 23219833 | Silencing OPG sensitized cells to TRAIL-induced apoptosis. |
| 425 | 23219833 | Interestingly, a positive correlation was noted between OPG production level and K-Ras mutation status. |
| 426 | 23219833 | Earlier studies implicated K-Ras in conferring resistance to TRAIL-induced apoptosis in pancreatic cells and this study demonstrates that K-Ras mediated TRAIL resistance in pancreatic cancer cells occurs due to increased OPG production. |
| 427 | 23219833 | Silencing K-Ras in pancreatic cancer cells decreased OPG levels and increased sensitivity to TRAIL-induced apoptosis. |
| 428 | 23219833 | These observations indicate that OPG can play a role in both cell survival and in PDAC cell sensitivity to TRAIL-induced apoptosis, which may contribute to metastasis. |
| 429 | 23219833 | Targeted inhibition of OPG binding to TRAIL may represent a therapeutic approach in the treatment of pancreatic cancer. |
| 430 | 23219833 | Mutations in K-Ras linked to levels of osteoprotegerin and sensitivity to TRAIL-induced cell death in pancreatic ductal adenocarcinoma cells. |
| 431 | 23219833 | Pancreatic ductal adenocarcinoma (PDAC) cell lines were found to secrete OPG and the level of OPG production correlated with sensitivity to TRAIL-induced apoptosis. |
| 432 | 23219833 | Silencing OPG sensitized cells to TRAIL-induced apoptosis. |
| 433 | 23219833 | Interestingly, a positive correlation was noted between OPG production level and K-Ras mutation status. |
| 434 | 23219833 | Earlier studies implicated K-Ras in conferring resistance to TRAIL-induced apoptosis in pancreatic cells and this study demonstrates that K-Ras mediated TRAIL resistance in pancreatic cancer cells occurs due to increased OPG production. |
| 435 | 23219833 | Silencing K-Ras in pancreatic cancer cells decreased OPG levels and increased sensitivity to TRAIL-induced apoptosis. |
| 436 | 23219833 | These observations indicate that OPG can play a role in both cell survival and in PDAC cell sensitivity to TRAIL-induced apoptosis, which may contribute to metastasis. |
| 437 | 23219833 | Targeted inhibition of OPG binding to TRAIL may represent a therapeutic approach in the treatment of pancreatic cancer. |
| 438 | 23219833 | Mutations in K-Ras linked to levels of osteoprotegerin and sensitivity to TRAIL-induced cell death in pancreatic ductal adenocarcinoma cells. |
| 439 | 23219833 | Pancreatic ductal adenocarcinoma (PDAC) cell lines were found to secrete OPG and the level of OPG production correlated with sensitivity to TRAIL-induced apoptosis. |
| 440 | 23219833 | Silencing OPG sensitized cells to TRAIL-induced apoptosis. |
| 441 | 23219833 | Interestingly, a positive correlation was noted between OPG production level and K-Ras mutation status. |
| 442 | 23219833 | Earlier studies implicated K-Ras in conferring resistance to TRAIL-induced apoptosis in pancreatic cells and this study demonstrates that K-Ras mediated TRAIL resistance in pancreatic cancer cells occurs due to increased OPG production. |
| 443 | 23219833 | Silencing K-Ras in pancreatic cancer cells decreased OPG levels and increased sensitivity to TRAIL-induced apoptosis. |
| 444 | 23219833 | These observations indicate that OPG can play a role in both cell survival and in PDAC cell sensitivity to TRAIL-induced apoptosis, which may contribute to metastasis. |
| 445 | 23219833 | Targeted inhibition of OPG binding to TRAIL may represent a therapeutic approach in the treatment of pancreatic cancer. |
| 446 | 23219833 | Mutations in K-Ras linked to levels of osteoprotegerin and sensitivity to TRAIL-induced cell death in pancreatic ductal adenocarcinoma cells. |
| 447 | 23219833 | Pancreatic ductal adenocarcinoma (PDAC) cell lines were found to secrete OPG and the level of OPG production correlated with sensitivity to TRAIL-induced apoptosis. |
| 448 | 23219833 | Silencing OPG sensitized cells to TRAIL-induced apoptosis. |
| 449 | 23219833 | Interestingly, a positive correlation was noted between OPG production level and K-Ras mutation status. |
| 450 | 23219833 | Earlier studies implicated K-Ras in conferring resistance to TRAIL-induced apoptosis in pancreatic cells and this study demonstrates that K-Ras mediated TRAIL resistance in pancreatic cancer cells occurs due to increased OPG production. |
| 451 | 23219833 | Silencing K-Ras in pancreatic cancer cells decreased OPG levels and increased sensitivity to TRAIL-induced apoptosis. |
| 452 | 23219833 | These observations indicate that OPG can play a role in both cell survival and in PDAC cell sensitivity to TRAIL-induced apoptosis, which may contribute to metastasis. |
| 453 | 23219833 | Targeted inhibition of OPG binding to TRAIL may represent a therapeutic approach in the treatment of pancreatic cancer. |
| 454 | 23219833 | Mutations in K-Ras linked to levels of osteoprotegerin and sensitivity to TRAIL-induced cell death in pancreatic ductal adenocarcinoma cells. |
| 455 | 23219833 | Pancreatic ductal adenocarcinoma (PDAC) cell lines were found to secrete OPG and the level of OPG production correlated with sensitivity to TRAIL-induced apoptosis. |
| 456 | 23219833 | Silencing OPG sensitized cells to TRAIL-induced apoptosis. |
| 457 | 23219833 | Interestingly, a positive correlation was noted between OPG production level and K-Ras mutation status. |
| 458 | 23219833 | Earlier studies implicated K-Ras in conferring resistance to TRAIL-induced apoptosis in pancreatic cells and this study demonstrates that K-Ras mediated TRAIL resistance in pancreatic cancer cells occurs due to increased OPG production. |
| 459 | 23219833 | Silencing K-Ras in pancreatic cancer cells decreased OPG levels and increased sensitivity to TRAIL-induced apoptosis. |
| 460 | 23219833 | These observations indicate that OPG can play a role in both cell survival and in PDAC cell sensitivity to TRAIL-induced apoptosis, which may contribute to metastasis. |
| 461 | 23219833 | Targeted inhibition of OPG binding to TRAIL may represent a therapeutic approach in the treatment of pancreatic cancer. |
| 462 | 23219833 | Mutations in K-Ras linked to levels of osteoprotegerin and sensitivity to TRAIL-induced cell death in pancreatic ductal adenocarcinoma cells. |
| 463 | 23219833 | Pancreatic ductal adenocarcinoma (PDAC) cell lines were found to secrete OPG and the level of OPG production correlated with sensitivity to TRAIL-induced apoptosis. |
| 464 | 23219833 | Silencing OPG sensitized cells to TRAIL-induced apoptosis. |
| 465 | 23219833 | Interestingly, a positive correlation was noted between OPG production level and K-Ras mutation status. |
| 466 | 23219833 | Earlier studies implicated K-Ras in conferring resistance to TRAIL-induced apoptosis in pancreatic cells and this study demonstrates that K-Ras mediated TRAIL resistance in pancreatic cancer cells occurs due to increased OPG production. |
| 467 | 23219833 | Silencing K-Ras in pancreatic cancer cells decreased OPG levels and increased sensitivity to TRAIL-induced apoptosis. |
| 468 | 23219833 | These observations indicate that OPG can play a role in both cell survival and in PDAC cell sensitivity to TRAIL-induced apoptosis, which may contribute to metastasis. |
| 469 | 23219833 | Targeted inhibition of OPG binding to TRAIL may represent a therapeutic approach in the treatment of pancreatic cancer. |
| 470 | 23401681 | Receptor activator of nuclear factor kappa-B ligand (RANKL) is not found in the vasculature in normal conditions, but may appear in calcifying areas. |
| 471 | 23401681 | OPG and RANKL are important regulators of mineral metabolism in both bone and vascular tissues. |
| 472 | 23401681 | Few data are available on the relationship between plasma OPG/RANKL levels and endothelial dysfunction as assessed using noninvasive methods like ultrasound indexes, neither in the general population nor, more specifically, in diabetic patients. |
| 473 | 23401681 | Receptor activator of nuclear factor kappa-B ligand (RANKL) is not found in the vasculature in normal conditions, but may appear in calcifying areas. |
| 474 | 23401681 | OPG and RANKL are important regulators of mineral metabolism in both bone and vascular tissues. |
| 475 | 23401681 | Few data are available on the relationship between plasma OPG/RANKL levels and endothelial dysfunction as assessed using noninvasive methods like ultrasound indexes, neither in the general population nor, more specifically, in diabetic patients. |
| 476 | 23456027 | This review provides an update on the mechanisms of vascular calcification including the emerging roles of the RANK/RANKL/OPG triad, osteoclasts, and microRNAs. |
| 477 | 23458176 | Association between osteoprotegerin, fetuin-A, carotid intima media thickness, and urinary albumin excretion in Type 2 diabetes. |
| 478 | 23607043 | In multivariate Cox regression analysis, the results showed that serum uric acid levels (odds ratio (OR) = 1.42, 95% CI = 1.20-1.82; P < 0.001), osteopontin (OR = 1.14, 95% CI = 1.12-1.25; P < 0.001), osteoprotegerin (OR = 1.45, 95% CI = 1.20-1.89; P < 0.001), type 2 diabetes mellitus (OR = 1.41, 95% CI = 1.20-1.72; P < 0.001), and total cholesterol (OR = 1.13, 95% CI = 1.10-1.22; P < 0.001) were factors that independently associated with coronary artery calcification. |
| 479 | 23652775 | In addition, treatment with CZE resulted in a significant increase in alkaline phosphatase (ALP) activity and collagen content, as well as in the expression of genes associated with osteoblast differentiation [ALP, collagen, osteopontin (OPN), osteoprotegerin (OPG), bone sialoprotein (BSP), osteocalcin (OC) and bone morphogenetic protein (BMP)2, BMP4 and BMP7]. |
| 480 | 23652775 | In mechanistic studies of the antioxidative potential of CZE, we found that CZE reversed the dRib-induced decrease in the expression of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT)1 and AKT2 genes, which are master regulators of survival-related signaling pathways. |
| 481 | 23652775 | CZE also upregulated the gene expression of the antioxidant enzymes, superoxide dismutase (SOD)2, SOD3 and glutathione peroxidase 4 (GPx4), which was inhibited by dRib. |
| 482 | 23758931 | Associations of fetuin-A and osteoprotegerin with arterial stiffness and early atherosclerosis in chronic hemodialysis patients. |
| 483 | 23816817 | The main mediators of such crosstalk include hormonal/cytokine signals from the bone (osteopontin, osteocalcin, and osteoprotegerin), the liver (fetuin-A), and adipose tissue [leptin, tumor necrosis factor-α (TNF-α), and adiponectin]. |
| 484 | 23871544 | GAGs were tested for their capability to bind to OPG and RANKL using surface plasmon resonance (SPR), ELISA and molecular modeling techniques. |
| 485 | 23871544 | Furthermore, OPG pre-incubated with different GAGs displayed a sulfate- and dose-dependent loss in bioactivity, possibly due to competition of GAGs for the RANKL/OPG binding site revealing a potential GAG interaction site at the RANKL/OPG interface. |
| 486 | 23871544 | In conclusion, high-sulfated GAGs might significantly control osteoclastogenesis via interference with the physiological RANKL/OPG complex formation. |
| 487 | 23871544 | GAGs were tested for their capability to bind to OPG and RANKL using surface plasmon resonance (SPR), ELISA and molecular modeling techniques. |
| 488 | 23871544 | Furthermore, OPG pre-incubated with different GAGs displayed a sulfate- and dose-dependent loss in bioactivity, possibly due to competition of GAGs for the RANKL/OPG binding site revealing a potential GAG interaction site at the RANKL/OPG interface. |
| 489 | 23871544 | In conclusion, high-sulfated GAGs might significantly control osteoclastogenesis via interference with the physiological RANKL/OPG complex formation. |
| 490 | 23871544 | GAGs were tested for their capability to bind to OPG and RANKL using surface plasmon resonance (SPR), ELISA and molecular modeling techniques. |
| 491 | 23871544 | Furthermore, OPG pre-incubated with different GAGs displayed a sulfate- and dose-dependent loss in bioactivity, possibly due to competition of GAGs for the RANKL/OPG binding site revealing a potential GAG interaction site at the RANKL/OPG interface. |
| 492 | 23871544 | In conclusion, high-sulfated GAGs might significantly control osteoclastogenesis via interference with the physiological RANKL/OPG complex formation. |
| 493 | 23874840 | Osteoprotegerin inhibits calcification of vascular smooth muscle cell via down regulation of the Notch1-RBP-Jκ/Msx2 signaling pathway. |
| 494 | 23877020 | Comparison of osteoprotegerin and vascular endothelial growth factor in normoalbuminuric Type 1 diabetic and control subjects. |
| 495 | 23934056 | The mRNA expression of ACE and renin receptor, and the protein expression of renin and angiotensin II were markedly up-regulated in the bone of vehicle-treated diabetic mice compared to those of non-diabetic mice, and these molecular changes of skeletal RAS components were effectively inhibited by treatment with captopril. |
| 496 | 23934056 | However, treatment with captopril significantly elevated serum tartrate-resistant acid phosphatase 5b levels, reduced the ratio of osteoprotegerin/receptor activator of nuclear factor-κB ligand expression, increased carbonic anhydrase II mRNA expression and the number of matured osteoclasts and decreased transforming growth factor-β and osteocalcin mRNA expression in the tibia compared to those of diabetic mice. |
| 497 | 23934086 | This cross-section study was designed to assess the effect of topical application of melatonin to the gingiva on salivary RANKL, osteoprotegrin (OPG) and melatonin levels as well as plasma melatonin in 30 patients with diabetes and periodontal disease and in a control group of 30 healthy subjects. |
| 498 | 23934086 | Salivary RANKL and OPG were measured by enzyme-linked immunosorbent assay and salivary and plasma melatonin by radioimmunoassay using commercial kits. |
| 499 | 23934086 | This cross-section study was designed to assess the effect of topical application of melatonin to the gingiva on salivary RANKL, osteoprotegrin (OPG) and melatonin levels as well as plasma melatonin in 30 patients with diabetes and periodontal disease and in a control group of 30 healthy subjects. |
| 500 | 23934086 | Salivary RANKL and OPG were measured by enzyme-linked immunosorbent assay and salivary and plasma melatonin by radioimmunoassay using commercial kits. |
| 501 | 23937044 | A direct correlation has been established between fetuin A and some adipokines involved in the formation of insulin resistance and atherogenesis (progranulin, omentin-1), and osteoprotegerin (the novel cardiovascular risk factor) as well as an increase of circulating levels of fetuin A in patients with type 2 diabetes mellitus with high cardiovascular risk metabolic pattern but without manifestations of macrovascular complications. |