Disease relevance of GFAP

• Although GFAP-like immunoreactivity was evident in glial cells of the proximal vestibular nerve, no immunoreactivity was detected in the distal portion of the vestibular nerve, vestibular ganglion, or vestibular end-organs [1].
• The activation of GFAP protein staining and metabolism in EAE might serve as a model for the activated growth of astrocyte processes which cause the severe gliosis seen in multiple sclerosis [2].
• After experimental detachment Müller cells quickly started to hypertrophy showing increased levels of intermediate filaments (i.e. vimentin and GFAP) [3].
• Immunocytochemical study of myelin-associated glycoprotein (MAG), basic protein (BP), and glial fibrillary acidic protein (GFAP) in chronic relapsing experimental allergic encephalomyelitis (EAE) [4].
• Vimentin, desmin, glial fibrillary acidic protein, neurofilament triplet proteins, and a mixture of cytokeratins were digested with Ca2+-activated neutral thiol proteinase isolated from Ehrlich ascites tumor (EAT) cells and porcine kidney [5].

High impact information on GFAP

• Amino acid sequence data on glial fibrillary acidic protein (GFA); implications for the subdivision of intermediate filaments into epithelial and non-epithelial members [6].
• Astrocytes, identified by their morphology and GFAP immunoreactivity, expressed very low levels of IGFBP-2 mRNA and peptide in normal controls; their levels were significantly higher 14 dpi, peaked 26 dpi, and then gradually decreased [7].
• The gene expression of both IGF-I and IGFBP-2 by hypertrophic GFAP-positive astrocytes was demonstrated 14-40 dpi by combined in situ hybridization and immunocytochemistry as well as by double immunostaining [7].
• Here, we describe the isolation of an evolutionary conserved novel GFAP isoform, GFAPkappa, produced by alternative splicing and polyadenylation of the 3'-region of the human GFAP pre-mRNA [8].
• Our results suggest that the relative expression level of the GFAPkappa isoform could modulate the properties of GFAP intermediate filaments and perhaps thereby influencing the motility of GFAP positive astrocytes and progenitor cells within the CNS [8].

Chemical compound and disease context of GFAP

• The percentage of injured neurons by hematoxylin and eosin staining and the degree of reactive astrocytosis by glial filbrillary acidic protein (GFAP) immunohistochemistry were assessed to determine histologic scores in the neocortex and hippocampus (0 = no injury to 4 = diffuse injury) [9].

Biological context of GFAP

• 3. The phosphorylation of GFAP was dependent on Ca2+ in the incubation medium in adult animals [10].
• As a consequence, the resulting human GFAPkappa protein harbors a nonconserved C-terminal tail sequence distinct from the tails of GFAPalpha, the predominant GFAP isoform, and GFAPepsilon, an isoform which also results from alternative splicing [8].

Anatomical context of GFAP

• In the monkey retina, GFAP-positive astrocytes were found ubiquitously in the NFL [11].
• Cochlear hair cells were not labeled for either GFAP or vimentin [12].
• Immunocytochemical techniques were used to look for the existence of two classes of intermediate filaments, vimentin and glial fibrillary acidic protein (GFAP), in cellular elements of the inner-ear epithelium in normal and experimentally damaged guinea-pig cochleas [12].
• The present study examined the immunocytochemical localization of various intermediate filaments (IFs), 68 kDa, 160 kDa and 200 kDa neurofilament protein (NFP), cytokeratin (CK) 1, 8, 10 and 19, vimentin, and glial fibrillary acidic protein (GFAP) in the vestibular end-organs and ganglia of normal and streptomycin-treated guinea pigs [1].
• 4. Both the immunocontent and level of phosphorylation of GFAP were higher in hippocampus than in cerebral cortex of all three species [10].

Associations of GFAP with chemical compounds

• Gentamicin (4%) was injected intratympanically into the middle ear of guinea pigs and the effects on the brainstem evaluated 28 days later by immunohistochemistry with an antibody against glial fibrillary acidic protein to detect astrocytes, and by cytochrome oxidase staining to detect metabolic activity [13].
• There were no intergroup differences regarding glial fibrillary acidic protein, neuron-specific enolase, S-100, interleukin-8, or substance P endopeptidase activity [14].

Other interactions of GFAP

• Astrocytes showing GFAP and vimentin immunoreactivity were absent from most of the horse retina [11].
• Primary cell cultures derived from striata of new-born piglets were set up and cells were characterized by immunocytochemistry using antibodies to neurofilament protein, a glial fibrillary acidic protein and a neuronal antigen recognized by a monoclonal antibody BM88 and by histochemistry for acetylcholinesterase [15].
• Concentrations of total proteins, the light subunit of the neurofilament protein, S-100 protein, neuron-specific enolase, and glial fibrillary acidic protein were measured, and the presence of oligoclonal bands (immunoglobulins) were assayed in cerebrospinal fluid [16].

Analytical, diagnostic and therapeutic context of GFAP

• Northern blot analysis using mouse GFAP DNA probe revealed that carp optic nerve RNA contains two transcripts of 2.3 and 2.1 kb, which hybridize with the mouse GFAP probe [17].
• Brain and spinal cord were stained by immunocytochemistry using W3/13 (T-lymphocytes) OX6 (MHC Class II) and GFAP (astrocytes) antibodies [18].
• Immunoprecipitation of GFAP with specific antiserum showed increased radioactivity in the complex beginning at day 10 when cellular infiltration was beginning in the EAE animals [2].
• The method is based on the detection of ruminant glial fibrillary acidic protein (GFAP) mRNA by applying real-time RT-PCR [19].
• The Schwann cell location of endopeptidase-24.11 was confirmed by correlation with immunostaining for glial fibrillary acidic protein and by electron microscopy [20].

References