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Articles in PresS, published online ahead of print October 2, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00210.2001
Submitted on July 6, 2001
Accepted on September 24, 2001
1 Kyoto Pharmaceutical University, Department of Pathological Biochemistry, Kyoto, Kyoto, Japan
* To whom correspondence should be addressed. E-mail: akiba{at}mb.kyoto-phu.ac.jp.
An increased prostaglandin production is implicated in the pathogenesis of glomerular diseases. In this respect, we examined the combined effect of reactive oxygen species and platelet-derived growth factor (PDGF), which might initiate glomerular dysfunction, on arachidonic acid release and cytosolic phospholipase A2 (cPLA2) activation in rat mesangial cells. H2O2-induced release of arachidonic acid was enhanced by PDGF, which by itself had little effect on the release, and the enhancement was completely inhibited by a cPLA2 inhibitor. The phosphorylation of cPLA2, extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein (MAP) kinase was up-regulated by H2O2 or PDGF alone, and except for ERK was enhanced further by the two in combination. The release of arachidonic acid induced by PDGF together with H2O2 was inhibited partially by an inhibitor of ERK or p38 MAP kinase, and completely when the two inhibitors were combined, the inhibitory pattern being similar to that for the phosphorylation of cPLA2. These results suggest that the ERK and p38 MAP kinase pathways are involved in the increase in cPLA2 activation and arachidonic acid release induced by PDGF together with H2O2.
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