Glial fibrillary acidic protein: GFAP-thirty-one years (1969-2000)

Citation
Lf. Eng et al., Glial fibrillary acidic protein: GFAP-thirty-one years (1969-2000), NEUROCHEM R, 25(9-10), 2000, pp. 1439-1451
Citations number
133
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROCHEMICAL RESEARCH
ISSN journal
03643190 → ACNP
Volume
25
Issue
9-10
Year of publication
2000
Pages
1439 - 1451
Database
ISI
SICI code
0364-3190(200010)25:9-10<1439:GFAPGY>2.0.ZU;2-M
Abstract
It is now well established that the glial fibrillary acidic protein (GFAP) is the principal 8-9 nm intermediate filament in mature astrocytes of the c entral nervous system (CNS). Over a decade ago, the value of GFAP as a prot otype antigen in nervous tissue identification and as a standard marker for fundamental and applied research at an interdisciplinary level was recogni zed (Raine, 135). As a member of the cytoskeletal protein family, GFAP is t hought to be important in modulating astrocyte motility and shape by provid ing structural stability to astrocytic processes. In the CNS of higher vert ebrates, following injury, either as a result of trauma, disease, genetic d isorders, or chemical insult, astrocytes become reactive and respond in a t ypical manner, termed astrogliosis. Astrogliosis is characterized by rapid synthesis of GFAP and is demonstrated by increase in protein content or by immunostaining with GFAP antibody. In addition to the major application of GFAP antisera for routine use in astrocyte identification in the CNS, the m olecular cloning of the mouse gene in 1985 has opened a new and rich realm for GFAP studies. These include antisense, null mice, and numerous promoter studies. Studies showing that mice lacking GFAP are hypersensitive to cerv ical spinal cord injury caused by sudden acceleration of the head have prov ided more direct evidence for a structural role of GFAP. While the structur al function of GFAP has become more acceptable, the use of GFAP antibodies and promoters continue to be valuable in studying CNS injury, disease, and development.