Disease relevance of GFAP

• The ratio of MBP to GFAP decreased (p < 0.05) as a function of ischemia, indicative of a proportionally greater loss of MBP than GFAP [1].
• The overexpression of GFAP gene could be related to a possible interaction between GFAP and scrapie infectious agent in astrocytes [2].
• Hypoxemic fetuses demonstrated severe gliosis in the cerebral cortex and reduced myelination of subcortical white matter as visualized by glial fibrillary acidic protein and myelin basic protein staining, respectively (p < 0.05) [3].
• Regional changes in kynurenic acid, quinolinic acid, and glial fibrillary acidic protein concentrations in the fetal sheep brain after experimentally induced placental insufficiency [4].

High impact information on GFAP

• Glial fibrillary acidic protein (GFAP) and isolectin B-4 immunoreactivity were used to label astrocytes and microglia, respectively [5].
• Insulin-like growth factor-1 treatment was associated with significantly reduced loss of oligodendrocytes in the intragyral white matter (P < 0.05), with improved MBP density (P < 0.05), reduced tissue swelling, and increased numbers of GFAP and isolectin B-4 positive cells compared with vehicle treatment [5].
• Ultrastructural homogeneity was not matched by the results of histochemical and immunohistochemical analysis: while all Type II cells stained positive to phosphotungstic acid hematoxylin, only 50% expressed glial fibrillary acidic protein [6].
• Filament proteins from non-keratinous tissues, such as desmin, vimentin, neurofilament proteins and the glial fibrillary acidic protein, which form monocomponent filaments, constitute a third type [7].
• We suggest that increased glial fibrillary acidic protein and 4-hydroxynonenal result from oxidative stress induced by QUIN, and that the increased intracellular albumin in cerebellar Purkinje cells may be an adaptive response [8].

Chemical compound and disease context of GFAP

• Expression of glial fibrillary acidic protein and glutamine synthetase genes in the natural scrapie of sheep [2].

Biological context of GFAP

• An up-regulation of genes related to glial activation (GFAP) and apoptosis (CASP3) was detected in obex and cerebrum, indicating a reactive glia [9].
• From 80 days of gestation onwards a continuous decrease of radial fibres occurred which was accompanied by an increase of GFAP-positive mature astrocytes [10].
• The topographical distribution of glial fibrillary acidic protein (GFAP), vimentin, neuron-specific enolase (NSE) and neurofilament (NF) proteins in the developing neocortex and cerebellum of sheep fetuses of different gestational ages (60-149 days) was described [10].
• Gene expression of two astroglial markers, glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS), was investigated in cerebellum and brainstem from scrapie-affected sheep [2].

Anatomical context of GFAP

• Eyes, optic nerves and brain from each animal were fixed and histologically processed using hematoxylin-eosin, followed by immunohistochemical staining for prion protein (PrPsc) and glial fibrillar acidic protein (GFAP) [11].
• Double immunolabelling demonstrated co-expression of BD viral antigen and glial fibrillary acidic protein (GFAP) or myelin basic protein (MBP) in both fetal and newborn lamb glia [12].
• Transverse semi-thin sections of the corpus callosum were cut and immuno-stained with antibody against glial fibrillary acidic protein (GFAP) [13].
• In Bergmann glial fibres of the cerebellum, which are the equivalent of radial fibres in the telencephalon, both GFAP and vimentin were detectable in fetuses and adult sheep [10].
• P450scc immunoreactivity was present in Purkinje neurons expressing either of the neuronal microtubule associated proteins MAP1b/5 or MAP2a/b, but was absent from GFAP and HNK-1 positive cells [14].

Associations of GFAP with chemical compounds

• OBJECTIVE: This study was undertaken to examine the effects of chronic embolization of the umbilical circulation during late gestation on regional concentrations of quinolinic acid and kynurenic acid (neuroactive products of tryptophan catabolism) and of the astrocyte-associated glial fibrillary acidic protein in the fetal brain [4].
• These markers were glial fibrillary acidic protein, myelin basic protein, myelin-associated glycoprotein, neuron-specific enolase, neurofilament protein, and fibronectin [15].
• Sagittal tissue sections were stained with toluidine blue and hematoxylin and eosin; Type IV collagen immunolocalization visualized blood vessel ingrowth, and nerves were immunolocalized using monoclonal antibodies to growth-associated protein (GAP-43), protein gene product 9.5, and glial fibrillary acidic protein [16].
• There was no significant difference in immunoreactivity for glial fibrillary acidic protein (GFAP) but it was more marked in the cerebellum of cocaine treated animals [17].

Other interactions of GFAP

• GLT1 protein expression within astrocytes is developmentally regulated, appearing first in vimentin positive radial glia at 60 and 71 days and then switching to GFAP positive parenchymal and perivascular astrocytes at 136 days [18].
• Immunolabelling with the nerve fibre markers PgP 9.5 and neuron-specific enolase and the satellite cell marker glial fibrillary acidic protein revealed the extensive ganglionated networks of the myenteric and submucosal plexi [19].

Analytical, diagnostic and therapeutic context of GFAP

• We investigated the expression of two markers of glial plasticity, glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS), by Western and Northern blotting, in different areas of the sheep brain [20].
• Optic nerve GFAP immunohistochemistry was performed and quantified [21].
• 1. The glial fibrillary acidic protein (GFAP) content of foetal, young (lamb) and adult sheep brain white (stem and cerebellum) and grey (cortex) matter-enriched regions has been determined by means of an improved ELISA using one layer of anti-human GFAP monoclonal antibody [22].
• Dual-label immunofluorescence using antibodies against glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) were used to characterize white matter lesions [1].

References