Bradykinin induces actin reorganization and enhances cell motility in HaCaT keratinocytes

被引:14
作者
Coutant, KD
Corvaia, N
Ryder, NS
机构
[1] NOVARTIS RES INST,DEPT GEN DERMATOL,A-1235 VIENNA,AUSTRIA
[2] NOVARTIS RES INST,DEPT IMMUNODERMATOL,A-1235 VIENNA,AUSTRIA
关键词
D O I
10.1006/bbrc.1997.7126
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In HaCaT keratinocytes bradykinin-triggered actin reorganization was inhibited by quinacrine, a phospholipase A(2) inhibitor, and restored by addition of arachidonic acid, Bradykinin-induced actin breakdown and cortical actin formation were respectively prevented by indomethacin, a cyclooxygenase inhibitor, and nordihydroguaiaretic acid, a lipoxygenase inhibitor. Addition of prostaglandins or leukotrienes, respectively, reversed the effects of inhibitors. This suggested a crucial role for a cyclooxygenase product in actin depolymerization and for a lipoxygenase product in cortical actin formation. Furthermore, we found that bradykinin stimulated HaCaT keratinocyte migration. This event was block;ed by quinacrine, indomethacin or nordihydroguaiaretic acid, and restored by addition of prostaglandins or leukotrienes, respectively. We also showed that genistein, a tyrosine kinase inhibitor, inhibited HaCaT cell locomotion. In conclusion, bradykinin modulated actin reorganization and cell motility in keratinocytes, probably by a mechanism involving arachidonic acid metabolites and a tyrosine kinase activity. (C) 1997 Academic Press.
引用
收藏
页码:257 / 261
页数:5
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