Premium
Proliferative and migratory responses of astrocytes to in vitro injury
Author(s) -
Környei Zsuzsanna,
Czirók András,
Vicsek Tamás,
Madarász Emilia
Publication year - 2000
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/1097-4547(20000815)61:4<421::aid-jnr8>3.0.co;2-4
Subject(s) - motility , in vitro , nestin , microbiology and biotechnology , astrocyte , wound healing , mitosis , cell , biology , scratch , chemistry , neuroscience , immunology , stem cell , neural stem cell , materials science , central nervous system , biochemistry , composite material
An in vitro “scratch‐wound” model was used to evoke and investigate some astroglial responses to mechanical injury. The changes in the morphology, locomotion, and proliferation of injured astrocytes were analysed under culture conditions devoid of blood‐derived cells responsible for activating the inflammatory cascade. The rate of proliferation was determined by immunocytochemical detection of BrdU‐incorporating cells located next to or far from the wound. The motility of individual cells and the mass‐advancement of cell‐assemblies were monitored by computer controlled video‐microscopy both in injured monolayers and in preparations of single cells or aggregates of astrocytes. The large sets of digitalized data allowed a reliable statistical evaluation of changes in cell positions providing a quantitative approach for studies on dynamics of cell locomotion. The results indicated that cultivated astrocytes respond to injury (1) with enhanced nestin immunoreactivity at the expanding processes, (2) with increased mitotic activity exceeding the rate caused by the liberation from contact inhibition, but (3) without specific, injury‐induced activation of cell locomotion. Some advantages and drawbacks of “scratch‐wound” models of astrocytic responses to mechanical injury are presented and discussed. J. Neurosci. Res. 61:421–429, 2000. © 2000 Wiley‐Liss, Inc.