Focal adhesion kinase is required for endothelin-induced cell cycle progression of cultured astrocytes
Article first published online: 14 MAY 2003
Copyright © 2003 Wiley-Liss, Inc.
Volume 43, Issue 2, pages 185–189, August 2003
How to Cite
Koyama, Y., Yoshioka, Y., Matsuda, T. and Baba, A. (2003), Focal adhesion kinase is required for endothelin-induced cell cycle progression of cultured astrocytes. Glia, 43: 185–189. doi: 10.1002/glia.10240
- Issue published online: 23 JUN 2003
- Article first published online: 14 MAY 2003
- Manuscript Accepted: 12 MAR 2003
- Manuscript Received: 25 JUN 2002
- Japan Society for the Promotion of Science
- Takeda Science Foundation
- actin organization
When the brain is damaged, astrocytes often cause hyperplasia resulting in glial scar formation at the injured sites. Endothelins (ETs) have been shown to be involved in the pathophysiologic responses of astrocytes, including proliferation. In this study, we examined the mechanisms underlying the ET-induced astrocytic G1/S-phase cell cycle transition by focusing on focal adhesion kinase (FAK). A transient transfection with wild-type FAK was followed by an increase in bromodeoxyuridine (BrdU) incorporation into cultured rat astrocytes. The increases in BrdU incorporation induced by 100 nM ET-1 were not found in astrocytes transfected with dominant-negative FAK mutants (FRNK and dC14-FAK). The increases in BrdU incorporation induced by 10 nM phorbol 12-myristate 13-acetate (PMA) were not affected by the FAK mutants. Wild-type FAK did not induce stress fiber formation in cultured astrocytes. The dominant negative FAK mutant dC14-FAK did not prevent ET-induced astrocytic stress fiber formation. These results suggest that FAK mediated the astrocytic G1/S cell cycle transition induced by ET-1 downstream of the cytoskeletal actin reorganization. © 2003 Wiley-Liss, Inc.