Abstract:
: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.
journal_name
Gliajournal_title
Gliaauthors
Koyama Y,Yoshioka Y,Matsuda T,Baba Adoi
10.1002/glia.10240subject
Has Abstractpub_date
2003-08-01 00:00:00pages
185-9issue
2eissn
0894-1491issn
1098-1136journal_volume
43pub_type
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