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

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

Research output: Contribution to journalArticlepeer-review

29 Scopus citations


The inflammatory cytokine interleukin-1β (IL-1β) 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-1β-induced NO and PGE2 biosynthesis in renal mesangial cells. We demonstrate that both insulin and IGF-I increase IL-1β-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-1β-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.

Original languageEnglish
Pages (from-to)F673-F679
JournalAmerican Journal of Physiology - Renal Physiology
Issue number4 43-4
StatePublished - Apr 1998


  • Cyclooxygenase
  • Mesangial cells
  • Nitric oxide synthase
  • Stress-activated protein kinase
  • p38 mitogen-activated protein kinase


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