Hydrogen peroxide-induced c-fos expression is mediated by arachidonic acid release: role of protein kinase C.
AUTOR(ES)
Rao, G N
RESUMO
We found previously that stimulation of c-fos and c-myc mRNA expression are early events in hydrogen peroxide-induced growth in rat aortic smooth muscle (RASM) cells. In the present study, we investigated the role of phospholipase A2 (PLA2) and protein kinase C (PKC) in mediating hydrogen peroxide-induced c-fos mRNA expression in RASM cells. Mepacrine and p-bromophenacylbromide, potent inhibitors of PLA2 activity, blocked hydrogen peroxide-induced c-fos mRNA expression. Arachidonic acid, a product of PLA2 activity, stimulated the expression of c-fos mRNA with a time course similar to that of hydrogen peroxide. PKC down-regulation attenuated both hydrogen peroxide and arachidonic acid-induced c-fos mRNA expression by 50%. Nordihydroguaiaretic acid (a lipoxygenase-cytochrome P450 monooxygenase inhibitor) significantly inhibited both hydrogen peroxide and arachidonic acid-induced c-fos mRNA expression, whereas indomethacin (a cyclooxygenase inhibitor) had no effect. Together, these findings indicate that 1) hydrogen peroxide-induced c-fos mRNA expression is mediated by PLA2-dependent arachidonic acid release, 2) both PKC-dependent and independent mechanisms are involved in hydrogen peroxide-induced expression of c-fos mRNA and 3) arachidonic acid metabolism via the lipoxygenase-cytochrome P450 monooxygenase pathway appears to be required for hydrogen peroxide-induced expression of c-fos mRNA.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=309291Documentos Relacionados
- A comprehensive analysis of hydrogen peroxide-induced gene expression in tobacco
- Potentiation by sulfide of hydrogen peroxide-induced killing of Escherichia coli.
- Repair of hydrogen peroxide-induced single-strand breaks in Escherichia coli deoxyribonucleic acid.
- A catalytic antioxidant metalloporphyrin blocks hydrogen peroxide-induced mitochondrial DNA damage
- Hydrogen peroxide-induced renal injury. A protective role for pyruvate in vitro and in vivo.