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Am J Physiol Renal Physiol 274: F673-F679, 1998;
0363-6127/98 $5.00
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Vol. 274, Issue 4, F673-F679, April 1998

IGF-I and insulin amplify IL-1beta -induced nitric oxide and prostaglandin biosynthesis

Zhonghong Guan, Shaavhree Y. Buckman, Lisa D. Baier, and Aubrey R. Morrison

Department of Molecular Biology and Pharmacology and Medicine, Washington University School of Medicine, St. Louis, Missouri 63110

The inflammatory cytokine interleukin-1beta (IL-1beta ) induces both cyclooxygenase-2 (Cox-2) and the inducible nitric oxide synthase (iNOS) with concomitant release of PGs and nitric oxide (NO) by glomerular mesangial cells. In our current studies, we determine whether insulin and IGF-I are involved in the signal transduction mechanisms resulting in IL-1beta -induced NO and PGE2 biosynthesis in renal mesangial cells. We demonstrate that both insulin and IGF-I increase IL-1beta -induced Cox-2 and iNOS protein expression, which in turn enhance PGE2 and NO production. Our data also indicate that both insulin and IGF-I enhance IL-1beta -induced p38 mitogen-activated protein kinase (MAPK) phosphorylation and SAPK activation. These findings implicate the possible role of the MAPK pathway in mediating the effects of insulin and IGF-I on the upregulation of cytokine-stimulated NO and PG biosynthesis. Together, our results indicate that IGF-I and insulin may function to modulate the renal inflammatory process.

p38 mitogen-activated protein kinase; stress-activated protein kinase; mesangial cells; cyclooxygenase; nitric oxide synthase


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