Studies on the molecular regulation of the inducible form of nitric oxide synthase (iNOS) in insulin-producing cells

Mol Cell Endocrinol. 1994 Dec;106(1-2):151-5. doi: 10.1016/0303-7207(94)90197-x.

Abstract

Nitric oxide, a radical generated by the enzyme nitric oxide synthase (iNOS), may be an important mediator of beta-cell damage in early insulin-dependent diabetes mellitus. We have investigated the molecular regulation of iNOS in insulin-producing RINm5F cells. The data obtained suggest that iNOS is maximally induced in these cells by a 6-h exposure to IL-1 beta or TNF-alpha + IFN-gamma, but not by endotoxin. iNOS mRNA degradation is rapid and it is not affected by IL-1 beta. Interestingly, NO seems to induce a negative feedback on iNOS expression, probably by decreasing iNOS transcription.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Oxidoreductases / biosynthesis
  • Amino Acid Oxidoreductases / genetics*
  • Animals
  • Enzyme Induction
  • Gene Expression Regulation*
  • Humans
  • Insulin / biosynthesis*
  • Insulinoma / enzymology*
  • Interferon-gamma / pharmacology
  • Interleukin-1 / pharmacology
  • Kinetics
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase
  • Pancreatic Neoplasms / enzymology*
  • RNA, Messenger / metabolism
  • Rats
  • Recombinant Proteins
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Insulin
  • Interleukin-1
  • RNA, Messenger
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • Interferon-gamma
  • Nitric Oxide Synthase
  • Amino Acid Oxidoreductases