PMID: 7539224May 11, 1995Paper

TGF-beta regulates production of NO in pulmonary artery smooth muscle cells by inhibiting expression of NOS

The American Journal of Physiology
J FinderP Davies

Abstract

We have previously reported that a mixture of lipopolysaccharide and cytokines stimulates cultured rat pulmonary artery smooth muscle cells (RPASM) to express elevated levels of mRNA for inducible nitric oxide synthase (iNOS), and to produce large amounts of nitric oxide (NO). The current study tests the hypothesis that transforming growth factor-beta (TGF-beta) modulates this process. Accordingly, RPASM were treated with a mixture of LPS (10 micrograms/ml) and the cytokines interleukin-1 beta (5 U/ml), tumor necrosis factor-alpha (500 U/ml), and interferon-gamma (100 U/ml). In the absence of TGF-beta 1, NO production (indicated by colorimetric assay of cumulative nitrite levels at 24 h) was greatly increased, as previously observed. Under identical conditions, TGF-beta 1 caused a concentration-dependent decrease in NO production. The addition of neither excess L-arginine nor sepiapterin reversed the inhibition, indicating that the effect of TGF-beta 1 was not due to limitation of enzyme substrate or cofactor tetrahydrobiopterin, respectively. Northern and Western analyses showed that TGF-beta 1 reduced levels of iNOS mRNA and protein to baseline at all time points examined up to 24 h. Complete suppression of iNOS protein expre...Continue Reading

Citations

Dec 22, 2009·American Journal of Physiology. Lung Cellular and Molecular Physiology·Patricia R BachillerJesse D Roberts
May 15, 2007·American Journal of Physiology. Lung Cellular and Molecular Physiology·Shilpa Vyas-ReadBrigham C Willis
Jun 15, 2011·American Journal of Physiology. Lung Cellular and Molecular Physiology·Letitia WeigandJ T Sylvester
Feb 3, 2012·Physiological Reviews·J T SylvesterJeremy P T Ward

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