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  • Title: IGF-I and insulin amplify IL-1 beta-induced nitric oxide and prostaglandin biosynthesis.
    Author: Guan Z, Buckman SY, Baier LD, Morrison AR.
    Journal: Am J Physiol; 1998 Apr; 274(4):F673-9. PubMed ID: 9575890.
    Abstract:
    The inflammatory cytokine interleukin-1 beta (IL-1 beta) 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-1 beta-induced NO and PGE2 biosynthesis in renal mesangial cells. We demonstrate that both insulin and IGF-I increase IL-1 beta-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-1 beta-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.
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