title: Role of GFAP in CNS injuries.
abstract: The role of GFAP in CNS injury is reviewed as revealed by studies using GFAP null mice. In order to provide background information for these studies, the effects of absence of GFAP in the uninjured astrocyte are also described. Activities attributable to GFAP include suppressing neuronal proliferation and neurite extension in the mature brain, forming a physical barrier to isolate damaged tissue, regulating blood flow following ischemia, contributing to the blood-brain barrier, supporting myelination, and providing mechanical strength. However, findings for many of these roles have been variable among laboratories, pointing to the presence of unappreciated complexity in GFAP function. One complexity may be regional differences in GFAP activities; others are yet to be discovered.
authors: Department of Neurobiology and the Civitan International Research Center, Center for Glial Biology in Medicine, Evelyn F. McKnight Brain Institute, University of Alabama at Birmingham, Birmingham, AL, United States. Electronic address: aaron@nrc.uab.edu.
authors: Michael
authors: M
authors: Brenner
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000473:pathology / Q000502:physiology; D001812:Blood-Brain Barrier / Q000378:metabolism; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002448:Cell Adhesion; D049109:Cell Proliferation; D005904:Glial Fibrillary Acidic Protein; D017774:Long-Term Potentiation; D036881:Long-Term Synaptic Depression; D018345:Mice, Knockout; D009186:Myelin Sheath / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D009474:Neurons / Q000473:pathology / Q000502:physiology; D014746:Vimentin / Q000378:metabolism
chemical_list: D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; D014746:Vimentin; C528900:glial fibrillary astrocytic protein, mouse
keywords: Astrocyte; CNS injury; GFAP; Ischemia; Neurotrauma; Reactive gliosis