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Gene Information
Gene symbol: GFAP
Gene name: glial fibrillary acidic protein
HGNC ID: 4235
Synonyms: FLJ45472
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1304218 | Microglial cells may be labeled by staining for LN-1, ricinus communis agglutinin-(RCA)-1, vimentin, HLA-DR-II, and nucleoside diphosphatase, but are negative for Leu-M1, Leu-M3, EBM-11, von Willebrand factor, CD22, cytokeratin, and glial fibrillary acidic protein (GFAP). |
| 2 | 1812289 | This study was performed to identify cellular components of the membranes by means of immunohistochemical technique. 11 proliferative vitreoretinal membranes which were surgically obtained from 7 eyes with PVR and 4 eyes with PDR were stained with monoclonal antibodies against cytokeratin, glial fibrillary acidic protein (GFAP), or vimentin using immunoperoxidase technique (ABC method). |
| 3 | 1812289 | In the PVR membranes, mean cell positivities for cytokeratin, GFAP and vimentin were 48%, 1% and 92%, respectively and in the PDR membranes, 0%, 5% and 93%, respectively. |
| 4 | 1812289 | This study was performed to identify cellular components of the membranes by means of immunohistochemical technique. 11 proliferative vitreoretinal membranes which were surgically obtained from 7 eyes with PVR and 4 eyes with PDR were stained with monoclonal antibodies against cytokeratin, glial fibrillary acidic protein (GFAP), or vimentin using immunoperoxidase technique (ABC method). |
| 5 | 1812289 | In the PVR membranes, mean cell positivities for cytokeratin, GFAP and vimentin were 48%, 1% and 92%, respectively and in the PDR membranes, 0%, 5% and 93%, respectively. |
| 6 | 1889766 | In addition, the topographic distribution of fibronectin was analyzed and the localization of the epidermal growth factor receptor, which is the coreceptor for the transforming growth factor alpha, was examined by staining procedures. |
| 7 | 1889766 | We used antibodies against macrophages (Ki-M7), cytokeratin, vimentin, desmin, glial fibrillary acidic protein and against the proliferation antigen Ki-67. |
| 8 | 1889766 | Among the cellular receptors necessary for signal transduction of mitogenic substances, we localized the coreceptor for the epidermal growth factor and the transforming growth factor alpha among actively proliferating macrophages in a PVR membrane. |
| 9 | 1915683 | The identification of microglia relies on positive labels for LN-1, Ricinus communis agglutinin-1, vimentin, HLA-DR, and nucleoside diphosphatase, and negative labels for Leu-M1, Leu-M3, EBM-11, von Willebrand factor, CD22, cytokeratin, and glial fibrillary acidic protein. |
| 10 | 2662103 | In MP membranes, most cells were GFAP-positive, whereas in PDR and PVR specimens, GFAP staining was variable. |
| 11 | 3947305 | Antisera against collagen types I, III, IV, and V, attachment factors fibronectin and laminin, endothelial marker factor VIII, and the glial-marker glial-fibrillary acidic protein were used to examined the membranes. |
| 12 | 7023612 | Glia cells of rat neural lobes (pituicytes) were stained in thin sections (6 micrometers) by the indirect immunofluorescence technique for the glial fibrillary acidic protein (GFA), the S-100 protein and fibronectin. |
| 13 | 8259261 | Antibodies against type I-IV collagen, fibronectin (FN), glial fibrillary acidic protein (GFAP), vimentin and the monoclonal antibody (MAB) against human Müller cells were used to examine the membranes. |
| 14 | 8259261 | The other types of collagen, FN and vimentin were also identified in most cases. |
| 15 | 8568932 | Immunolocalization of GLUT1 and GLUT3 glucose transporters in primary cultured neurons and glia. |
| 16 | 8568932 | Immunofluorescence analysis was used to study the cellular localization of glucose transporters 1 and 3 (GLUT1 and GLUT3) in primary rat neuronal and glial cultures. |
| 17 | 8568932 | GLUT3 distribution corresponded most closely with the neural cell adhesion molecule (NCAM), and showed overlapping but distinct distributions compared to synaptophysin, microtubule-associated protein 2 (MAP2), neurofilament protein, and growth-associated protein (GAP43). |
| 18 | 8568932 | GLUT1, but not GLUT3, was detected in glial fibrillary acidic protein (GFAP)-positive astrocytes present in mixed neuronal-glial cultures derived from cerebellum and cerebral cortex, as well as in cortical astrocyte cultures. |
| 19 | 8741254 | Immunohistochemical studies showed positive reaction for S-100 protein in the tumor cell nuclei, but no reaction for glial fibrillary acidic protein, neurofilament protein, Leu-7, oxytocin, beta-endorphin, adrenocorticotropic hormone, and vimentin. |
| 20 | 9519752 | In this study, we sought evidence for diabetes-induced Müller cell abnormalities by testing the expression of three proteins (Bcl-2, glutamine synthetase [GS], and glial fibrillar acidic protein [GFAP]) that are solely or predominantly expressed in Müller cells and show a reproducible pattern of changes in the context of retinal injuries or degenerations. |
| 21 | 9878779 | Neomycin (10-250 nmol) produced dose-dependent striatal damage manifested as an increased gliosis as measured by: (1) [3H]PK-11195 binding, (2) staining for the astrocytic marker glial fibrillary acidic protein (GFAP) and (3) staining for OX-6, an MHC class II antigen expressed by microglia and macrophages. |
| 22 | 10219959 | These alterations were accompanied by a significantly elevated mean numerical density of astrocytes (positive for glial fibriallary acidic protein; GFAP+) within the periventricular hypothalamic area (PER) of the insulin-treated rats (P < 0.05). |
| 23 | 10219959 | These observations speak for a varying vulnerability of LHA, DMN and distinct parts of the VMN to hyperinsulinism during early development, possibly leading to a disturbed organization and, consecutively, permanent dysfunction of these morphologically connected and functionally interacting hypothalamic nuclei. |
| 24 | 10433248 | Finally, electrophoretic mobility shift assays using nuclear extracts from neural cells revealed the presence of IDX1/IPF1 bound to a putative homeodomain protein DNA-binding site present in the promoter of the glial fibrillary acidic protein gene. |
| 25 | 11006253 | Altered expression of retinal occludin and glial fibrillary acidic protein in experimental diabetes. |
| 26 | 11532429 | In the nerve fibre and ganglion cell layers, astrocytes expressed both glial fibrillary acidic protein and ET-1 proteins suggesting that these cells may secrete ET-1. |
| 27 | 11532429 | Expression of ETA and ETB receptors in human retina were demonstrated by reverse transcription-polymerase chain reaction. |
| 28 | 12107504 | Nestin is an intermediate filament protein expressed by neuroepithelial stem cells and which has been proposed to represent also a marker for putative islet stem cells. |
| 29 | 12107504 | These cells also expressed desmin, vimentin, and glial fibrillary acidic protein which are known to represent stellate cell markers. |
| 30 | 12360045 | Immunohistochemically, all lesions were KP1 (CD68) and vimentin positive and lysozyme, S-100 protein, HMB-45, epithelial membrane antigen, cytokeratins, factor VIIIrag, CD34, muscle-specific actin, alpha-smooth muscle actin, desmin (D33), desmin (Der-11), chromogranin, synaptophysin, neurofilament protein, and glial fibrillary acidic protein negative. |
| 31 | 12453501 | While METH caused dopaminergic nerve terminal degeneration as indicated by decreased striatal dopamine (49%) and tyrosine hydroxylase protein (68%), as well as an increase in glial fibrillary acidic protein by 313% in the lean mice, these effects were exacerbated under the obese condition (96%, 86% and 602%, respectively). |
| 32 | 12539039 | Pancreatic islets of Langerhans are enveloped by peri-islet Schwann cells (pSC), which express glial fibrillary acidic protein (GFAP) and S100beta. pSC-autoreactive T- and B-cell responses arise in 3- to 4-week-old diabetes-prone non-obese diabetic (NOD) mice, followed by progressive pSC destruction before detectable beta-cell death. |
| 33 | 12539039 | Moreover, GFAP-specific NOD T-cell lines transferred pathogenic peri-insulitis to NOD/severe combined immunodeficient (NOD/SCID) mice, and immunotherapy with GFAP or S100beta prevented diabetes. pSC survived in rat insulin promoter Iymphocytic choriomeningitis virus (rip-LCMV) glycoprotein/CD8+ T-cell receptor(gp) double-transgenic mice with virus-induced diabetes, suggesting that pSC death is not an obligate consequence of local inflammation and beta-cell destruction. |
| 34 | 12539039 | Pancreatic islets of Langerhans are enveloped by peri-islet Schwann cells (pSC), which express glial fibrillary acidic protein (GFAP) and S100beta. pSC-autoreactive T- and B-cell responses arise in 3- to 4-week-old diabetes-prone non-obese diabetic (NOD) mice, followed by progressive pSC destruction before detectable beta-cell death. |
| 35 | 12539039 | Moreover, GFAP-specific NOD T-cell lines transferred pathogenic peri-insulitis to NOD/severe combined immunodeficient (NOD/SCID) mice, and immunotherapy with GFAP or S100beta prevented diabetes. pSC survived in rat insulin promoter Iymphocytic choriomeningitis virus (rip-LCMV) glycoprotein/CD8+ T-cell receptor(gp) double-transgenic mice with virus-induced diabetes, suggesting that pSC death is not an obligate consequence of local inflammation and beta-cell destruction. |
| 36 | 12540628 | Diabetic mice, known to have much lower aldose reductase activity in other tissues when compared with rats, did not accumulate sorbitol and fructose in the retina and were protected from neuronal apoptosis and GFAP changes in the presence of GHb levels of 14 +/- 2%. |
| 37 | 12591097 | Increase of glial fibrillary acidic protein and S-100B in hippocampus and cortex of diabetic rats: effects of vitamin E. |
| 38 | 12591097 | One of the important events during astrocyte differentiation is the increased expression of glial markers, glial fibrillary acidic protein (GFAP) and S-100B protein. |
| 39 | 12591097 | In the present study, we aimed to investigate glial reactivity in hippocampus, cortex and cerebellum of streptozotocin-induced diabetic rats by determining the expression of GFAP and S-100B and also to examine the protective effects of vitamin E against gliosis. |
| 40 | 12591097 | Western blotting showed increases in total and degraded GFAP content and S-100B protein expression in brain tissues of diabetic rats compared with those of controls. |
| 41 | 12591097 | These findings indicate that streptozotocin-induced diabetes alters degradation and production of GFAP and S-100B, which are markers of reactive astrocytosis. |
| 42 | 12591097 | Thus, determination of GFAP and S-100B may provide a relevant marker in the central nervous system for studying neurodegenerative changes in experimental diabetes mellitus. |
| 43 | 12591097 | Increase of glial fibrillary acidic protein and S-100B in hippocampus and cortex of diabetic rats: effects of vitamin E. |
| 44 | 12591097 | One of the important events during astrocyte differentiation is the increased expression of glial markers, glial fibrillary acidic protein (GFAP) and S-100B protein. |
| 45 | 12591097 | In the present study, we aimed to investigate glial reactivity in hippocampus, cortex and cerebellum of streptozotocin-induced diabetic rats by determining the expression of GFAP and S-100B and also to examine the protective effects of vitamin E against gliosis. |
| 46 | 12591097 | Western blotting showed increases in total and degraded GFAP content and S-100B protein expression in brain tissues of diabetic rats compared with those of controls. |
| 47 | 12591097 | These findings indicate that streptozotocin-induced diabetes alters degradation and production of GFAP and S-100B, which are markers of reactive astrocytosis. |
| 48 | 12591097 | Thus, determination of GFAP and S-100B may provide a relevant marker in the central nervous system for studying neurodegenerative changes in experimental diabetes mellitus. |
| 49 | 12591097 | Increase of glial fibrillary acidic protein and S-100B in hippocampus and cortex of diabetic rats: effects of vitamin E. |
| 50 | 12591097 | One of the important events during astrocyte differentiation is the increased expression of glial markers, glial fibrillary acidic protein (GFAP) and S-100B protein. |
| 51 | 12591097 | In the present study, we aimed to investigate glial reactivity in hippocampus, cortex and cerebellum of streptozotocin-induced diabetic rats by determining the expression of GFAP and S-100B and also to examine the protective effects of vitamin E against gliosis. |
| 52 | 12591097 | Western blotting showed increases in total and degraded GFAP content and S-100B protein expression in brain tissues of diabetic rats compared with those of controls. |
| 53 | 12591097 | These findings indicate that streptozotocin-induced diabetes alters degradation and production of GFAP and S-100B, which are markers of reactive astrocytosis. |
| 54 | 12591097 | Thus, determination of GFAP and S-100B may provide a relevant marker in the central nervous system for studying neurodegenerative changes in experimental diabetes mellitus. |
| 55 | 12591097 | Increase of glial fibrillary acidic protein and S-100B in hippocampus and cortex of diabetic rats: effects of vitamin E. |
| 56 | 12591097 | One of the important events during astrocyte differentiation is the increased expression of glial markers, glial fibrillary acidic protein (GFAP) and S-100B protein. |
| 57 | 12591097 | In the present study, we aimed to investigate glial reactivity in hippocampus, cortex and cerebellum of streptozotocin-induced diabetic rats by determining the expression of GFAP and S-100B and also to examine the protective effects of vitamin E against gliosis. |
| 58 | 12591097 | Western blotting showed increases in total and degraded GFAP content and S-100B protein expression in brain tissues of diabetic rats compared with those of controls. |
| 59 | 12591097 | These findings indicate that streptozotocin-induced diabetes alters degradation and production of GFAP and S-100B, which are markers of reactive astrocytosis. |
| 60 | 12591097 | Thus, determination of GFAP and S-100B may provide a relevant marker in the central nervous system for studying neurodegenerative changes in experimental diabetes mellitus. |
| 61 | 12591097 | Increase of glial fibrillary acidic protein and S-100B in hippocampus and cortex of diabetic rats: effects of vitamin E. |
| 62 | 12591097 | One of the important events during astrocyte differentiation is the increased expression of glial markers, glial fibrillary acidic protein (GFAP) and S-100B protein. |
| 63 | 12591097 | In the present study, we aimed to investigate glial reactivity in hippocampus, cortex and cerebellum of streptozotocin-induced diabetic rats by determining the expression of GFAP and S-100B and also to examine the protective effects of vitamin E against gliosis. |
| 64 | 12591097 | Western blotting showed increases in total and degraded GFAP content and S-100B protein expression in brain tissues of diabetic rats compared with those of controls. |
| 65 | 12591097 | These findings indicate that streptozotocin-induced diabetes alters degradation and production of GFAP and S-100B, which are markers of reactive astrocytosis. |
| 66 | 12591097 | Thus, determination of GFAP and S-100B may provide a relevant marker in the central nervous system for studying neurodegenerative changes in experimental diabetes mellitus. |
| 67 | 12591097 | Increase of glial fibrillary acidic protein and S-100B in hippocampus and cortex of diabetic rats: effects of vitamin E. |
| 68 | 12591097 | One of the important events during astrocyte differentiation is the increased expression of glial markers, glial fibrillary acidic protein (GFAP) and S-100B protein. |
| 69 | 12591097 | In the present study, we aimed to investigate glial reactivity in hippocampus, cortex and cerebellum of streptozotocin-induced diabetic rats by determining the expression of GFAP and S-100B and also to examine the protective effects of vitamin E against gliosis. |
| 70 | 12591097 | Western blotting showed increases in total and degraded GFAP content and S-100B protein expression in brain tissues of diabetic rats compared with those of controls. |
| 71 | 12591097 | These findings indicate that streptozotocin-induced diabetes alters degradation and production of GFAP and S-100B, which are markers of reactive astrocytosis. |
| 72 | 12591097 | Thus, determination of GFAP and S-100B may provide a relevant marker in the central nervous system for studying neurodegenerative changes in experimental diabetes mellitus. |
| 73 | 14583344 | Key indicators of this response are increased synthesis of glial fibrillary acidic protein (GFAP) and S100B, both astrocytic markers. |
| 74 | 14583344 | In the present study, we examined glial reactivity in hippocampus, cortex, and cerebellum of streptozotocin (STZ)-induced diabetic rats by determining the expression of GFAP and S-100B and we evaluated the effect of melatonin on the glial response. |
| 75 | 14583344 | Like GFAP, S100B levels also were increased in all three brain areas of diabetic rats, an effect also reduced by melatonin treatment. |
| 76 | 14583344 | Key indicators of this response are increased synthesis of glial fibrillary acidic protein (GFAP) and S100B, both astrocytic markers. |
| 77 | 14583344 | In the present study, we examined glial reactivity in hippocampus, cortex, and cerebellum of streptozotocin (STZ)-induced diabetic rats by determining the expression of GFAP and S-100B and we evaluated the effect of melatonin on the glial response. |
| 78 | 14583344 | Like GFAP, S100B levels also were increased in all three brain areas of diabetic rats, an effect also reduced by melatonin treatment. |
| 79 | 14583344 | Key indicators of this response are increased synthesis of glial fibrillary acidic protein (GFAP) and S100B, both astrocytic markers. |
| 80 | 14583344 | In the present study, we examined glial reactivity in hippocampus, cortex, and cerebellum of streptozotocin (STZ)-induced diabetic rats by determining the expression of GFAP and S-100B and we evaluated the effect of melatonin on the glial response. |
| 81 | 14583344 | Like GFAP, S100B levels also were increased in all three brain areas of diabetic rats, an effect also reduced by melatonin treatment. |
| 82 | 15111491 | These impaired responses were associated with the destruction of 3v tanycytes, reduced glial fibrillary acidic protein-immunoreactivity surrounding the 3v, neuronal swelling, and decreased arcuate nucleus neuropeptide Y (NPY) mRNA. |
| 83 | 15111491 | At this time there were significant decreases in GK, NPY, and proopiomelanocortin mRNA. |
| 84 | 15378652 | We examined the effects of streptozotocin (STZ)-induced diabetes in rats on the level of the astrocyte intermediate filament protein, glial fibrillary acidic protein (GFAP), number of astrocytes, and levels of the astrocyte glutamate transporters, glutamate transporter-1 (GLT-1) and glutamate/aspartate transporter (GLAST), in the cerebral cortex, hippocampus, and cerebellum by Western blotting (WB) and immunohistochemistry (IH). |
| 85 | 15521814 | The expression of glial fibrillary acidic protein (GFAP), S100B protein, and neuron specific enolase (NSE) was determined as well as lipid peroxidation (LPO) and glutathione (GSH) levels in some brain tissues. |
| 86 | 15521814 | Western blot analyses showed GFAP, S100B, and NSE levels significantly increased under STZ-induced diabetes in brain, and LPO level increased as well. |
| 87 | 15521814 | The expression of glial fibrillary acidic protein (GFAP), S100B protein, and neuron specific enolase (NSE) was determined as well as lipid peroxidation (LPO) and glutathione (GSH) levels in some brain tissues. |
| 88 | 15521814 | Western blot analyses showed GFAP, S100B, and NSE levels significantly increased under STZ-induced diabetes in brain, and LPO level increased as well. |
| 89 | 15800711 | The aim of our study was to determine whether synthetic ligands of PPARalpha and PPARgamma could affect the viability, proliferation, differentiation, apoptosis and expression of some cell cycle related proteins in glial tumor cell lines. |
| 90 | 15800711 | Cell lines were treated by ligands of PPARalpha (bezafibrate, gemfibrozil) and PPARgamma (ciglitazone). |
| 91 | 15800711 | The synthetic ligands significantly reduced or induced the expression of cyclins, p27Kip1, p21Waf1/Cip1, MDM-2, Bcl-2, Bax, PARP, Caspase 3, androgen receptors, etc. and did not affect the expression of the differentiation marker GFAP. |
| 92 | 15961235 | In AD cortical brain region, somatostatin and neuropeptide-Y-positive neurons decreased (>70%), and glial fibrillary acidic protein-positive astrocytes significantly increased (>130%) in comparison to control brain. |
| 93 | 15961235 | SSTR2 and 4 were the predominant subtypes followed by SSTR1, 3 and 5. |
| 94 | 15961235 | AD cortex showed a marked reduction in neuronal expression of SSTR4 and 5 and a modest decrease in SSTR2-like immunoreactivity without any changes in SSTR1 immunoreactive neurons. |
| 95 | 15961235 | In AD cortex, SSTR1-, 3- and 4-like immunoreactivities were strongly expressed in glial cells but not SSTR2 and 5. |
| 96 | 15961235 | These findings suggest the differential loss of immunoreactivity of SSTR2, 4 and 5 but not SSTR1, and increased SSTR3 in frontal cortex of AD brain as well as subtype-selective glial expression in AD brain. |
| 97 | 16178982 | In this study, our goal was to (i) calculate the microvessel density (MVD), (ii) evaluate vascular endothelial growth factor (VEGF) expression and (iii) correlate angiogenesis with the proliferative activity as expressed by the expression of Ki67 marker, in both membrane types. |
| 98 | 16178982 | We performed immunohistochemistry in 14 PVR and eight PDR membranes, using antibodies against CD34, VEGF, Ki67 and glial fibrillary acidic protein. |
| 99 | 16178982 | The expression of Ki67 was not correlated with microvessel number or VEGF expression. |
| 100 | 16340083 | Insulin and insulin-like growth factor expression and function deteriorate with progression of Alzheimer's disease: link to brain reductions in acetylcholine. |
| 101 | 16340083 | Glucose utilization and energy metabolism are regulated by insulin and insulin-like growth factor I (IGF-I), and correspondingly, studies have shown that cognitive impairment may be improved by glucose or insulin administration. |
| 102 | 16340083 | Recently, we demonstrated significantly reduced levels of insulin and IGF-I polypeptide genes and their corresponding receptors in advanced AD relative to aged control brains. |
| 103 | 16340083 | Realtime quantitative RT-PCR analysis of frontal lobe tissue demonstrated that increasing AD Braak Stage was associated with progressively reduced levels of mRNA corresponding to insulin, IGF-I, and IGF-II polypeptides and their receptors, tau, which is regulated by insulin and IGF-I, and the Hu D neuronal RNA binding protein. |
| 104 | 16340083 | In contrast, progressively increased levels of amyloid beta protein precursor (AbetaPP), glial fibrillary acidic protein, and the IBA1/AIF1 microglial mRNA transcripts were detected with increasing AD Braak Stage. |
| 105 | 16340083 | Impairments in growth factor and growth factor receptor expression and function were associated with increasing AD Braak stage dependent reductions in insulin, IGF-I, and IGF-II receptor binding, ATP levels, and choline acetyltransferase (ChAT) expression. |
| 106 | 16340083 | Further studies demonstrated that: 1) ChAT expression increases with insulin or IGF-I stimulation; 2) ChAT is expressed in insulin and IGF-I receptor-positive cortical neurons; and 3) ChAT co-localization in insulin or IGF-I receptor-positive neurons is reduced in AD. |
| 107 | 16374706 | We used immunohistochemistry and immunoblotting from untreated control and streptozotocin-induced type 1 (insulin dependent) diabetic rats to investigate main olfactory epithelial mitotic rate and glial fibrillary acidic protein expression in the lamina propria of the sensory epithelium and in the olfactory bulb. |
| 108 | 16453021 | GDNF rescues hyperglycemia-induced diabetic enteric neuropathy through activation of the PI3K/Akt pathway. |
| 109 | 16453021 | Exposure to 20 mM glucose resulted in decreased Akt phosphorylation and enhanced nuclear translocation of forkhead box O3a (FOXO3a). |
| 110 | 16453021 | The pathophysiological effects of hyperglycemia (apoptosis, reduced Akt phosphorylation, loss of inhibitory neurons, motility changes) were reversed in diabetic glial fibrillary acidic protein-GDNF (GFAP-GDNF) Tg mice. |
| 111 | 16627931 | More recently, studies with human postmortem brain tissue linked many of the characteristic molecular and pathological features of AD to reduced expression of the insulin and insulin-like growth factor (IGF) genes and their corresponding receptors. |
| 112 | 16627931 | The ic-STZ-injected rats did not have elevated blood glucose levels, and pancreatic architecture and insulin immunoreactivity were similar to control, yet their brains were reduced in size and exhibited neurodegeneration associated with cell loss, gliosis, and increased immunoreactivity for p53, active glycogen synthase kinase 3beta, phospho-tau, ubiquitin, and amyloid-beta. |
| 113 | 16627931 | Real time quantitative RT-PCR studies demonstrated that the ic-STZ-treated brains had significantly reduced expression of genes corresponding to neurons, oligodendroglia, and choline acetyltransferase, and increased expression of genes encoding glial fibrillary acidic protein, microglia-specific proteins, acetylcholinesterase, tau, and amyloid precursor protein. |
| 114 | 16627931 | These abnormalities were associated reduced expression of genes encoding insulin, IGF-II, insulin receptor, IGF-I receptor, and insulin receptor substrate-1, and reduced ligand binding to the insulin and IGF-II receptors. |
| 115 | 16753303 | Colocalization of glial fibrillary acidic protein (GFAP) and cleaved caspase 3 and GFAP in TUNEL-positive cells increased in diabetic rats. |
| 116 | 16753303 | Changes in GFAP levels paralleled modifications in proliferating cell nuclear antigen (PCNA), increasing at 1 week of diabetes and decreasing thereafter, and proliferating GFAP-positive cells were decreased in the cerebellum of diabetic rats. |
| 117 | 16753303 | Colocalization of glial fibrillary acidic protein (GFAP) and cleaved caspase 3 and GFAP in TUNEL-positive cells increased in diabetic rats. |
| 118 | 16753303 | Changes in GFAP levels paralleled modifications in proliferating cell nuclear antigen (PCNA), increasing at 1 week of diabetes and decreasing thereafter, and proliferating GFAP-positive cells were decreased in the cerebellum of diabetic rats. |
| 119 | 16926846 | In situ hybridization using bfl-1 (microglia) and glial fibrillary acidic protein (GFAP) (astrocytes) revealed expression of both bfl-1 and GFAP in the ipsilateral hemisphere at 4 h in the db/+ mice, which was delayed and minimal in the db/db mice. |
| 120 | 16926846 | RNase protection assays showed a robust increase in expression of the proinflammatory cytokines tumor necrosis factor-alpha (TNFalpha), interleukin-1 IL-1alpha, and IL-1beta mRNA in the db/+ mice at 6 to 8 h of reperfusion peaking at 8 to 12 h; in db/db mice expression was markedly delayed and diminished. |
| 121 | 16926846 | Real-time-polymerase chain reaction (RT-PCR) confirmed the reduced and delayed expression TNFalpha, IL-1alpha, IL-1beta, and the growth factors insulin-like growth factor-1 and ciliary neurotrophic factor in the db/db mice; enzyme-linked immunosorbent assays confirmed the reduced and delayed translation of IL-1beta protein. |
| 122 | 16979383 | We have identified for the first time an age-dependent spontaneous loss of tolerance to two self-antigenic epitopes derived from putative diabetes-associated antigens glutamic acid decarboxylase (GAD65) and glial fibrillary acidic protein (GFAP) in RIP-B7/DRB1*0404 HLA transgenic mice. |
| 123 | 16979383 | Diabetic and older non-diabetic mice exhibited a proliferative response to an immunodominant epitope from GAD65 (555-567) and also from GFAP (240-252) but not from an immunogenic epitope from diabetes-associated islet-specific glucose-6-phosphatase catalytic subunit-related protein. |
| 124 | 16979383 | Islet infiltrates in older non-diabetic mice and diabetic mice contain CD4(+)/FoxP3(+) cells and suggest the presence of a regulatory mechanism prior and during diabetic disease. |
| 125 | 16979383 | We have identified for the first time an age-dependent spontaneous loss of tolerance to two self-antigenic epitopes derived from putative diabetes-associated antigens glutamic acid decarboxylase (GAD65) and glial fibrillary acidic protein (GFAP) in RIP-B7/DRB1*0404 HLA transgenic mice. |
| 126 | 16979383 | Diabetic and older non-diabetic mice exhibited a proliferative response to an immunodominant epitope from GAD65 (555-567) and also from GFAP (240-252) but not from an immunogenic epitope from diabetes-associated islet-specific glucose-6-phosphatase catalytic subunit-related protein. |
| 127 | 16979383 | Islet infiltrates in older non-diabetic mice and diabetic mice contain CD4(+)/FoxP3(+) cells and suggest the presence of a regulatory mechanism prior and during diabetic disease. |
| 128 | 17065343 | In an effort to identify novel epitopes, we used matrix-assisted algorithms to predict peptides of glial fibrillary acidic protein (GFAP), prepro-islet amyloid polypeptide (ppIAPP), and islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) that likely bind to HLA-A*0201 with a strong affinity and contain a COOH-terminal proteasomal cleavage site. |
| 129 | 17065343 | Seven peptides stabilized HLA-A*0201 expression in binding assays and were used to stimulate peripheral blood mononuclear cells and were evaluated for granzyme B secretion. |
| 130 | 17065343 | Other peptides recognized by type 1 diabetic or antibody-positive subjects included GFAP(143-151), IGRP(152-160), and GFAP(214-222). |
| 131 | 17065343 | These data implicate peptides of ppIAPP, GFAP, and IGRP as CTL epitopes for a heterogenous CD8(+) T-cell response in type 1 subjects and antibody-positive relatives. |
| 132 | 17065343 | In an effort to identify novel epitopes, we used matrix-assisted algorithms to predict peptides of glial fibrillary acidic protein (GFAP), prepro-islet amyloid polypeptide (ppIAPP), and islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) that likely bind to HLA-A*0201 with a strong affinity and contain a COOH-terminal proteasomal cleavage site. |
| 133 | 17065343 | Seven peptides stabilized HLA-A*0201 expression in binding assays and were used to stimulate peripheral blood mononuclear cells and were evaluated for granzyme B secretion. |
| 134 | 17065343 | Other peptides recognized by type 1 diabetic or antibody-positive subjects included GFAP(143-151), IGRP(152-160), and GFAP(214-222). |
| 135 | 17065343 | These data implicate peptides of ppIAPP, GFAP, and IGRP as CTL epitopes for a heterogenous CD8(+) T-cell response in type 1 subjects and antibody-positive relatives. |
| 136 | 17065343 | In an effort to identify novel epitopes, we used matrix-assisted algorithms to predict peptides of glial fibrillary acidic protein (GFAP), prepro-islet amyloid polypeptide (ppIAPP), and islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) that likely bind to HLA-A*0201 with a strong affinity and contain a COOH-terminal proteasomal cleavage site. |
| 137 | 17065343 | Seven peptides stabilized HLA-A*0201 expression in binding assays and were used to stimulate peripheral blood mononuclear cells and were evaluated for granzyme B secretion. |
| 138 | 17065343 | Other peptides recognized by type 1 diabetic or antibody-positive subjects included GFAP(143-151), IGRP(152-160), and GFAP(214-222). |
| 139 | 17065343 | These data implicate peptides of ppIAPP, GFAP, and IGRP as CTL epitopes for a heterogenous CD8(+) T-cell response in type 1 subjects and antibody-positive relatives. |
| 140 | 18329889 | Ganglioside GM1 effects on the expression of nerve growth factor (NGF), Trk-A receptor, proinflammatory cytokines and on autoimmune diabetes onset in non-obese diabetic (NOD) mice. |
| 141 | 18329889 | In the present study, serum, pancreas islets and spleen mononuclear cells from NOD mice treated with monosialic ganglioside GM1 (100 mg/kg/day) and the group control which received saline solution were isolated to investigate the proinflammatory cytokines (IL-1beta, IFN-gamma, IL-12, TNF-alpha), NGF and its high-affinity receptor TrkA, peri-islet Schwann cells components (GFAP, S100-beta) expression and the relationship with diabetes onset and morphological aspects. |
| 142 | 18329889 | Our results suggest that GM1 administration to female NOD mice beginning at the 4th week of life is able to reduce the index of inflammatory infiltrate and consequently the expression of diabetes, modulating the expression of proinflammatory cytokines (IL-12, IFN-gamma, TNF-alpha and IL-1beta). |
| 143 | 18329889 | Furthermore, GM1 increases GFAP, S-100beta and NGF in pancreas islets, factors involved in beta cell survival. |
| 144 | 18329889 | Ganglioside GM1 effects on the expression of nerve growth factor (NGF), Trk-A receptor, proinflammatory cytokines and on autoimmune diabetes onset in non-obese diabetic (NOD) mice. |
| 145 | 18329889 | In the present study, serum, pancreas islets and spleen mononuclear cells from NOD mice treated with monosialic ganglioside GM1 (100 mg/kg/day) and the group control which received saline solution were isolated to investigate the proinflammatory cytokines (IL-1beta, IFN-gamma, IL-12, TNF-alpha), NGF and its high-affinity receptor TrkA, peri-islet Schwann cells components (GFAP, S100-beta) expression and the relationship with diabetes onset and morphological aspects. |
| 146 | 18329889 | Our results suggest that GM1 administration to female NOD mice beginning at the 4th week of life is able to reduce the index of inflammatory infiltrate and consequently the expression of diabetes, modulating the expression of proinflammatory cytokines (IL-12, IFN-gamma, TNF-alpha and IL-1beta). |
| 147 | 18329889 | Furthermore, GM1 increases GFAP, S-100beta and NGF in pancreas islets, factors involved in beta cell survival. |
| 148 | 18563560 | Blood glucose content, content of taurine, glutamate and <gamma>-amino butyric acid (GABA) and expression of glial fibrillary acid protein (GFAP), vascular endothelial growth factor (VEGF), glutamate transporter (GLAST), glutamine synthetase (GS) and glutamate decarboxylase (GAD) in retina were determined in diabetic rats fed without or with 5% taurine in a controlled trial lasting 12 weeks, with normal rats fed without or with 5% taurine served as controls. |
| 149 | 18563560 | With supplementation of taurine in diet, lower expression of GFAP and VEGF while higher expression of GLAST, GS and GAD in retina of diabetic rats were determinated by RT-PCR, Western-blotting and immunofluorescence (P < 0.05). |
| 150 | 18563560 | GFAP, VEGF, GLAST, GS and GAD expressions in normal controls were not altered by taurine treatment. |
| 151 | 18563560 | Blood glucose content, content of taurine, glutamate and <gamma>-amino butyric acid (GABA) and expression of glial fibrillary acid protein (GFAP), vascular endothelial growth factor (VEGF), glutamate transporter (GLAST), glutamine synthetase (GS) and glutamate decarboxylase (GAD) in retina were determined in diabetic rats fed without or with 5% taurine in a controlled trial lasting 12 weeks, with normal rats fed without or with 5% taurine served as controls. |
| 152 | 18563560 | With supplementation of taurine in diet, lower expression of GFAP and VEGF while higher expression of GLAST, GS and GAD in retina of diabetic rats were determinated by RT-PCR, Western-blotting and immunofluorescence (P < 0.05). |
| 153 | 18563560 | GFAP, VEGF, GLAST, GS and GAD expressions in normal controls were not altered by taurine treatment. |
| 154 | 18563560 | Blood glucose content, content of taurine, glutamate and <gamma>-amino butyric acid (GABA) and expression of glial fibrillary acid protein (GFAP), vascular endothelial growth factor (VEGF), glutamate transporter (GLAST), glutamine synthetase (GS) and glutamate decarboxylase (GAD) in retina were determined in diabetic rats fed without or with 5% taurine in a controlled trial lasting 12 weeks, with normal rats fed without or with 5% taurine served as controls. |
| 155 | 18563560 | With supplementation of taurine in diet, lower expression of GFAP and VEGF while higher expression of GLAST, GS and GAD in retina of diabetic rats were determinated by RT-PCR, Western-blotting and immunofluorescence (P < 0.05). |
| 156 | 18563560 | GFAP, VEGF, GLAST, GS and GAD expressions in normal controls were not altered by taurine treatment. |
| 157 | 18708122 | Astrocyte count, size and shape as well as levels of glial fibrillary acidic protein (GFAP) and S100b protein were assessed 3, 7 and 14 days after the STZ injection using immunohistochemistry, immuno-enzyme assay and computer-assisted image analysis. |
| 158 | 18780965 | In a C57BL/6 mouse model of obesity and T2DM, we characterized the histopathology, gene expression, and insulin and insulin-like growth factor (IGF)-receptor binding in temporal lobe. |
| 159 | 18780965 | These effects were associated with significantly increased levels of tau, IGF-I receptor, insulin receptor substrate-1 (IRS-1), IRS-4, ubiquitin, glial fibrillary acidic protein, and 4-hydroxynonenol, and decreased expression of beta-actin. |
| 160 | 18784648 | After 11 days, these STZ-diabetic mice showed increased glucocorticoid secretion and hippocampal alterations characterized by: (1) increased glial fibrillary acidic protein-positive astrocytes as a marker reacting to neurodegeneration, (2) increased c-Jun expression marking neuronal activation, (3) reduced Ki-67 immunostaining indicating decreased cell proliferation. |
| 161 | 19227273 | Immunohistochemical (tests for insulin, glucagons, periferin, SNAP-25, GFAP, NGF-R, RMR-22, MBP) and morphological studies were performed to examine the pancreatic nervous apparatus of human adults and fetuses in late phases of development. |
| 162 | 19227273 | The insular endocrine cells are shown to synthesize the proteins (SNAP-25, GFAP) characteristic of nerve cells and their synaptic terminals. |
| 163 | 19227273 | Immunohistochemical (tests for insulin, glucagons, periferin, SNAP-25, GFAP, NGF-R, RMR-22, MBP) and morphological studies were performed to examine the pancreatic nervous apparatus of human adults and fetuses in late phases of development. |
| 164 | 19227273 | The insular endocrine cells are shown to synthesize the proteins (SNAP-25, GFAP) characteristic of nerve cells and their synaptic terminals. |
| 165 | 19748503 | The expression of GFAP and AQPs 1 and 4 was assessed by immunohistochemistry of cryosections and retinal flatmounts. |
| 166 | 19784582 | Interestingly, the levels of iNOS and GFAP were increased in the gallbladders of cholesterol-fed hamsters. |
| 167 | 19812959 | Immunohistochemical studies, confirmed by Western blot analysis, demonstrated the enhancement of vimentin and GFAP immunoreactivity (IR) in astrocytes located in the perilesion cortical area of the diabetic rats that were operated upon. |
| 168 | 19861974 | In this study, we investigated the actions of the peroxisome proliferator-activated receptor (PPAR)-gamma agonist darglitazone in treating diabetes and promoting recovery after a hypoxic-ischemic (H/I) insult in the diabetic ob/ob mouse. |
| 169 | 19861974 | Microglial and astrocytic activation monitored by cytokine expression (interleukin-1beta and tumor necrosis factor-alpha) and in situ hybridization studies (bfl1 and glial fibrillary acidic protein) suggest a biphasic inflammatory response, with darglitazone restoring the compromised proinflammatory response(s) in the diabetic mouse at 4 h but suppressing subsequent inflammatory responses at 8 and 24 h in both control and diabetic mice. |
| 170 | 19890475 | Targets of S100A1 include proteins involved in calcium signaling (ryanidine receptors 1 & 2, Serca2a, phopholamban), neurotransmitter release (synapsins I & II), cytoskeletal and filament associated proteins (CapZ, microtubules, intermediate filaments, tau, mocrofilaments, desmin, tubulin, F-actin, titin, and the glial fibrillary acidic protein GFAP), transcription factors and their regulators (e.g. myoD, p53), enzymes (e.g. aldolase, phosphoglucomutase, malate dehydrogenase, glycogen phosphorylase, photoreceptor guanyl cyclases, adenylate cyclases, glyceraldehydes-3-phosphate dehydrogenase, twitchin kinase, Ndr kinase, and F1 ATP synthase), and other Ca2+-activated proteins (annexins V & VI, S100B, S100A4, S100P, and other S100 proteins). |
| 171 | 21652728 | Fetal neonatal leptin and insulin deficiency results in reduced hypothalamic axonal pathways regulating appetite, which may predispose to offspring hyperphagia and obesity. |
| 172 | 21652728 | Neural development of the arcuate nucleus, a key target of adiposity signals, leptin and insulin, is immature at birth. |
| 173 | 21652728 | Hence, to explore proximate effects of leptin/insulin on hypothalamic development, we determined trophic and differentiation effects on neural stem/progenitor cells using a model of fetal hypothalamic neurospheres (NS). |
| 174 | 21652728 | NS cultures were produced from embryonic d 20 fetal rats and passage 1 and passage 2 cells examined for proliferation and differentiation into neurons (neuronal nuclei, class IIIβ-tubulin, and doublecortin) and astrocytes (glial fibrillary acidic protein). |
| 175 | 21652728 | Leptin-induced NS proliferation was significantly greater than that induced by insulin, although both effects were blocked by Notch, extracellular signal-regulated kinase, or signal transducer and activator of transcription 3 inhibition. |
| 176 | 21652728 | Leptin preferentially induced neuronal, whereas insulin promoted astrocyte differentiation. |
| 177 | 21652728 | Extracellular signal-regulated kinase inhibition suppressed both leptin and insulin-mediated differentiation, whereas signal transducer and activator of transcription inhibition only affected leptin-mediated responses. |
| 178 | 21652728 | Altered fetal exposure to leptin or insulin, resulting from fetal growth restriction, macrosomia, or maternal diabetes, may potentially have marked effects on fetal brain development. |
| 179 | 21712075 | RU486 (mifepristone) ameliorates cognitive dysfunction and reverses the down-regulation of astrocytic N-myc downstream-regulated gene 2 in streptozotocin-induced type-1 diabetic rats. |
| 180 | 21712075 | However, the role for chronically elevated glucocorticoids and hippocampal astrocytic activations in DCD remains to be elucidated, and it is not clear whether astrocytic N-myc downstream-regulated gene 2 (NDRG2, involved in cell differentiation and development) participated in DCD. |
| 181 | 21712075 | Diabetic rats also presented down-regulation of glial fibrillary acidic protein (GFAP, a key indicator of astrocytic reactivity) and NDRG2 in hippocampus revealed by immunohistochemistry staining, real-time PCR and Western blot. |
| 182 | 21712075 | Moreover, the diabetic cognitive impairments were ameliorated by 9-day glucocorticoids receptor (GR) blockade with RU486, and the down-regulation of hippocampal NDRG2 and GFAP in diabetic animals was also attenuated by 9-day GR blockade. |
| 183 | 21712075 | RU486 (mifepristone) ameliorates cognitive dysfunction and reverses the down-regulation of astrocytic N-myc downstream-regulated gene 2 in streptozotocin-induced type-1 diabetic rats. |
| 184 | 21712075 | However, the role for chronically elevated glucocorticoids and hippocampal astrocytic activations in DCD remains to be elucidated, and it is not clear whether astrocytic N-myc downstream-regulated gene 2 (NDRG2, involved in cell differentiation and development) participated in DCD. |
| 185 | 21712075 | Diabetic rats also presented down-regulation of glial fibrillary acidic protein (GFAP, a key indicator of astrocytic reactivity) and NDRG2 in hippocampus revealed by immunohistochemistry staining, real-time PCR and Western blot. |
| 186 | 21712075 | Moreover, the diabetic cognitive impairments were ameliorated by 9-day glucocorticoids receptor (GR) blockade with RU486, and the down-regulation of hippocampal NDRG2 and GFAP in diabetic animals was also attenuated by 9-day GR blockade. |
| 187 | 22178606 | We report here that high glucose (HG) treatment stimulated astrocytic morphological alteration coupled with changes in glial fibrillary acidic protein (GFAP) and vimentin expression. |
| 188 | 22178606 | Additionally, HG upregulated the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), interleukin-4 (IL-4), and vascular endothelial growth factor (VEGF); however, its effects on transforming growth factor-β (TGF-β) expression were not evident. |
| 189 | 22178606 | HG treatment induced increased production of reactive oxygen species (ROS) as well as activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and signal transducer and activator transcription 3 (STAT 3). |
| 190 | 22178606 | HG-induced expression of TNF-α, IL-6, IL-1β, IL-4, and VEGF was blocked by ROS scavenger and inhibitors specific for NF-κB and STAT 3, respectively. |
| 191 | 22202163 | Unlike activin A, CnP inhibited activation of cultured stellate cells and reduced the production of collagen. |
| 192 | 22202163 | In pancreatic sections obtained from 6-wk-old GK rats, CD68-positive macrophages and glial fibrillary acidic protein- and α-smooth muscle actin-positive stellate cells infiltrated into islets. |
| 193 | 22554865 | Retinal function (electroretinogram, ERG) and morphology (optical microscopy), retinal nitric oxide synthase (NOS) activity (using (3)H-arginine), lipid peroxidation (thiobarbituric acid reactive substances, TBARS), and TNFα levels (ELISA) were evaluated. |
| 194 | 22554865 | At 12 weeks of treatment, a significant decrease in the ERG a- and b- wave and oscillatory potential amplitudes, and a significant increase in retinal NOS activity, TBARS, TNFα, glial fibrillary acidic protein in Müller cells, and vascular endothelial growth factor levels were observed. |
| 195 | 22711212 | Angiotensin-(1-7) via the mas receptor alleviates the diabetes-induced decrease in GFAP and GAP-43 immunoreactivity with concomitant reduction in the COX-2 in hippocampal formation: an immunohistochemical study. |
| 196 | 22711212 | We examined the effect of Ang-(1-7) on the number of cyclooxygenase-2 (COX-2) immunoreactive neurons and the glial fibrillary acidic protein (GFAP)-immunoreactive astrocytes and assessed the changes in the neuronal growth-associated protein-43 (GAP-43) of the hippocampal formation in streptozotocin-induced diabetes in rats. |
| 197 | 22711212 | Ang-(1-7) treatment significantly prevented diabetes-induced decrease in the number of GFAP immunoreactive astrocytes and GAP-43 positive neurons in all hippocampal regions. |
| 198 | 22711212 | Angiotensin-(1-7) via the mas receptor alleviates the diabetes-induced decrease in GFAP and GAP-43 immunoreactivity with concomitant reduction in the COX-2 in hippocampal formation: an immunohistochemical study. |
| 199 | 22711212 | We examined the effect of Ang-(1-7) on the number of cyclooxygenase-2 (COX-2) immunoreactive neurons and the glial fibrillary acidic protein (GFAP)-immunoreactive astrocytes and assessed the changes in the neuronal growth-associated protein-43 (GAP-43) of the hippocampal formation in streptozotocin-induced diabetes in rats. |
| 200 | 22711212 | Ang-(1-7) treatment significantly prevented diabetes-induced decrease in the number of GFAP immunoreactive astrocytes and GAP-43 positive neurons in all hippocampal regions. |
| 201 | 22711212 | Angiotensin-(1-7) via the mas receptor alleviates the diabetes-induced decrease in GFAP and GAP-43 immunoreactivity with concomitant reduction in the COX-2 in hippocampal formation: an immunohistochemical study. |
| 202 | 22711212 | We examined the effect of Ang-(1-7) on the number of cyclooxygenase-2 (COX-2) immunoreactive neurons and the glial fibrillary acidic protein (GFAP)-immunoreactive astrocytes and assessed the changes in the neuronal growth-associated protein-43 (GAP-43) of the hippocampal formation in streptozotocin-induced diabetes in rats. |
| 203 | 22711212 | Ang-(1-7) treatment significantly prevented diabetes-induced decrease in the number of GFAP immunoreactive astrocytes and GAP-43 positive neurons in all hippocampal regions. |
| 204 | 22891211 | Compared with vehicle-treated DBA/STZ/WD mice, GW3965 treated mice showed fewer acellular capillaries and reduced GFAP expression. |
| 205 | 22946773 | Melatonin, which did not affect glucose metabolism in control or diabetic rats, prevented the decrease in the electroretinogram a-wave, b-wave, and oscillatory potential amplitude, and the increase in retinal lipid peroxidation, NOS activity, TNFα, Müller cells glial fibrillary acidic protein, and vascular endothelial growth factor levels. |
| 206 | 23153579 | Ischemic pulses reduced the decrease in the electroretinogram a-wave, b-wave, and oscillatory potential amplitude, and the increase in retinal lipid peroxidation, NOS activity, TNFα, Müller cells glial fibrillary acidic protein, and vascular endothelial growth factor levels observed in diabetic animals. |
| 207 | 23376836 | The Hsp treatment (100 mg/kg body weight) was carried for twenty four weeks in STZ-induced diabetic rats and evaluated for antioxidant (Superoxide dismutase; SOD, Catalase; CAT and glutathione; GSH) enzymes, inflammatory cytokines (TNF-α, IL-1β), caspase-3, glial fibrillary acidic protein (GFAP) and aquaporin-4(AQP4) expression. |
| 208 | 23376836 | Diabetic retinae showed increased caspase-3, GFAP and AQP4 expression. |
| 209 | 23376836 | However, Hsp-treated retinae showed inhibitory effect on caspase-3, GFAP and AQP4 expression. |
| 210 | 23376836 | The Hsp treatment (100 mg/kg body weight) was carried for twenty four weeks in STZ-induced diabetic rats and evaluated for antioxidant (Superoxide dismutase; SOD, Catalase; CAT and glutathione; GSH) enzymes, inflammatory cytokines (TNF-α, IL-1β), caspase-3, glial fibrillary acidic protein (GFAP) and aquaporin-4(AQP4) expression. |
| 211 | 23376836 | Diabetic retinae showed increased caspase-3, GFAP and AQP4 expression. |
| 212 | 23376836 | However, Hsp-treated retinae showed inhibitory effect on caspase-3, GFAP and AQP4 expression. |
| 213 | 23376836 | The Hsp treatment (100 mg/kg body weight) was carried for twenty four weeks in STZ-induced diabetic rats and evaluated for antioxidant (Superoxide dismutase; SOD, Catalase; CAT and glutathione; GSH) enzymes, inflammatory cytokines (TNF-α, IL-1β), caspase-3, glial fibrillary acidic protein (GFAP) and aquaporin-4(AQP4) expression. |
| 214 | 23376836 | Diabetic retinae showed increased caspase-3, GFAP and AQP4 expression. |
| 215 | 23376836 | However, Hsp-treated retinae showed inhibitory effect on caspase-3, GFAP and AQP4 expression. |
| 216 | 23536314 | Immunofluorescence staining and Western blotting demonstrated that cilostazol treatment reduced GFAP and VEGF expression in the retinas of OLETF rats. |
| 217 | 23545209 | Similar findings were found in the hippocampus, where an increased number of GFAP immunoreactive astrocytes were detected in the CA1 and CA3 subfields and dentate gyrus of OZRs compared to the LZRs. |
| 218 | 23584706 | Our immunohistochemistry approach has shown that the insulin receptor, insulin receptor substrate 1 (IRS1), protein kinase B (PKB) and insulin-sensitive glucose transporter (GLUT4) are expressed in the sensory epithelium of the human saccule, which also exhibits expression of a calcium-sensitive cAMP/cGMP phosphodiesterase 1C (PDE1C) and the vasopressin type 2 receptor. |
| 219 | 23584706 | IRS1 and PDE1C are selectively expressed in sensory epithelial hair cells, whereas the other components are expressed in sensory epithelial supporting cells or in both cell types, as judged from co-expression or non-co-expression with glial fibrillary acidic protein, a marker for supporting cells. |
| 220 | 23584706 | Furthermore, IRS1 appears to be localized in association with sensory nerves, whereas GLUT4 is expressed in the peri-nuclear area of stromal cells, as is the case for aquaporin 2. |
| 221 | 23667870 | Autoantibodies to neuron-specific proteins S100, GFAP, MBP and NGF in the serum of rats with streptozotocin-induced diabetes. |
| 222 | 23667870 | The appearance of autoantibodies to neuronal proteins (S100, GFAP, MBP, and NGF) in rat serum was analyzed by ELISA on days 5, 10, 17, 25, and 32 after streptozotocin injection. |
| 223 | 23667870 | The levels of antibodies to specific neuronal proteins (S100, GFAP, MBP, and NGF) also increased at this term. |
| 224 | 23667870 | Autoantibodies to neuron-specific proteins S100, GFAP, MBP and NGF in the serum of rats with streptozotocin-induced diabetes. |
| 225 | 23667870 | The appearance of autoantibodies to neuronal proteins (S100, GFAP, MBP, and NGF) in rat serum was analyzed by ELISA on days 5, 10, 17, 25, and 32 after streptozotocin injection. |
| 226 | 23667870 | The levels of antibodies to specific neuronal proteins (S100, GFAP, MBP, and NGF) also increased at this term. |
| 227 | 23667870 | Autoantibodies to neuron-specific proteins S100, GFAP, MBP and NGF in the serum of rats with streptozotocin-induced diabetes. |
| 228 | 23667870 | The appearance of autoantibodies to neuronal proteins (S100, GFAP, MBP, and NGF) in rat serum was analyzed by ELISA on days 5, 10, 17, 25, and 32 after streptozotocin injection. |
| 229 | 23667870 | The levels of antibodies to specific neuronal proteins (S100, GFAP, MBP, and NGF) also increased at this term. |
| 230 | 23726157 | Diabetes and obesity were monitored in C57Bl/6J mice fed a 72% high-fat diet, and duodenal glial expression patterns were evaluated by immunohistochemistry and RT-PCR for S100β, Sox10 and GFAP proteins and transcripts, as well as transmission electron microscopy (TEM). |
| 231 | 16868181 | We have demonstrated, in rats with streptozotocin-induced diabetes, that mechanical hyperalgesia, a common symptom of diabetic neuropathy, was correlated with an early increase in extracellular signal-regulated protein kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) phosphorylation in the spinal cord and dorsal root ganglion at 3 weeks after induction of diabetes. |
| 232 | 16868181 | In diabetic hyperalgesic rats, immunocytochemistry revealed that all phosphorylated mitogen-activated protein kinases (MAPKs) colocalized with both the neuronal (NeuN) and microglial (OX42) cell-specific markers but not with the astrocyte marker [glial fibrillary acidic protein (GFAP)] in the superficial dorsal horn-laminae of the spinal cord. |
| 233 | 16868181 | In these same rats, a 7-day administration [5 microg/rat/day, intrathecal (i.t.)] of 1,4-diamino-2,3-dicyano-1,4-bis(2-aminophenylthio)butadiene (U0126), 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580), and anthra(1,9-cd)pyrazol-6(2H)-one (SP600125), which inhibited MAPK kinase, p38, and JNK, respectively, suppressed mechanical hyperalgesia, and decreased phosphorylation of the kinases. |