Kd. Coutant et al., BRADYKININ INDUCES ACTIN REORGANIZATION AND ENHANCES CELL MOTILITY INHACAT KERATINOCYTES, Biochemical and biophysical research communications, 237(2), 1997, pp. 257-261
In HaCaT keratinocytes bradykinin-triggered actin reorganization was i
nhibited by quinacrine, a phospholipase A(2) inhibitor, and restored b
y addition of arachidonic acid, Bradykinin-induced actin breakdown and
cortical actin formation were respectively prevented by indomethacin,
a cyclooxygenase inhibitor, and nordihydroguaiaretic acid, a lipoxyge
nase inhibitor. Addition of prostaglandins or leukotrienes, respective
ly, reversed the effects of inhibitors. This suggested a crucial role
for a cyclooxygenase product in actin depolymerization and for a lipox
ygenase product in cortical actin formation. Furthermore, we found tha
t bradykinin stimulated HaCaT keratinocyte migration. This event was b
lock;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 reorg
anization and cell motility in keratinocytes, probably by a mechanism
involving arachidonic acid metabolites and a tyrosine kinase activity.
(C) 1997 Academic Press.