Effects of transforming growth factor-beta 1 on nitric oxide synthesis by C2C12 skeletal myocytes

Am J Physiol. 1996 Jan;270(1 Pt 2):R145-52. doi: 10.1152/ajpregu.1996.270.1.R145.

Abstract

The production of nitric oxide (NO) via the inducible form of NO synthase (iNOS) is regulated by a complex network of cytokines and endogenous hormones. Among these, transforming growth factor-beta (TGF-beta 1) is known to suppress iNOS expression and NO production by many cell types. To determine the effect of TGF-beta 1 on NO production by skeletal muscle cells, we stimulated C2C12 myocytes with interferon-gamma (IFN) and interleukin-1 (IL-1) in the presence or absence of TGF-beta 1. In contrast to findings in macrophages, TGF-beta 1 markedly enhanced NO production by skeletal muscle cells. Increases in NO production reflected significant increases in iNOS immunoreactive protein and iNOS mRNA. Elevated iNOS mRNA levels associated with TGF-beta 1 treatment were not due to an alteration in mRNA stability, but rather reflected a significantly increased transcriptional rate of the iNOS gene. These findings indicate that TGF-beta 1 enhances iNOS expression in skeletal muscle cells and suggest that the regulation of NO production by TGF-beta 1 may depend on the cell type studied.

MeSH terms

  • Animals
  • Cell Differentiation
  • Cell Line
  • Cytokines / pharmacology
  • Drug Synergism
  • Half-Life
  • Mice
  • Mice, Inbred C3H
  • Muscle, Skeletal / cytology
  • Muscle, Skeletal / metabolism*
  • Nitric Oxide / biosynthesis*
  • Nitric Oxide Synthase / biosynthesis
  • Nitric Oxide Synthase / genetics
  • Nitrites / metabolism
  • RNA, Messenger / metabolism
  • Transcription, Genetic
  • Transforming Growth Factor beta / pharmacology*

Substances

  • Cytokines
  • Nitrites
  • RNA, Messenger
  • Transforming Growth Factor beta
  • Nitric Oxide
  • Nitric Oxide Synthase