Hydrogen sulfide potentiates interleukin-1beta-induced nitric oxide production via enhancement of extracellular signal-regulated kinase activation in rat vascular smooth muscle cells.

Authors: Jeong SO (1) , Pae HO (1) , Oh GS (1) , Jeong GS (1) , Lee BS (1) , Lee S (2) , Kim DY (3) , Rhew HY (3) , Lee KM (4) , Chung HT (1)
(1) Medicinal Resources Research Institute, Wonkwang University, Department of Microbiology and Immunology, Wonkwang University School of Medicine (2) Department of Pharmacology, Wonkwang University School of Medicine (3) Department of Urology, College of Medicine, Kosin University (4) Division of Biological Science, College of Natural Science, Chonbuk National University
Source: Biochem Biophys Res Commun. 2006 Jul 7;345(3):938-44.
DOI: 10.1016/j.bbrc.2006.05.002 Publication date: 2006 Jul E-Publication date: May 8, 2006 Availability: abstract Copyright: © 2006 Published by Elsevier Inc.
Language: English Countries: Not specified Location: Not specified Correspondence address: Chung HT : htchung@wonkwang.ac.kr


Article abstract

Hydrogen sulfide (H(2)S) and nitric oxide (NO) are endogenously synthesized from l-cysteine and l-arginine, respectively. They might constitute a cooperative network to regulate their effects. In this study, we investigated whether H(2)S could affect NO production in rat vascular smooth muscle cells (VSMCs) stimulated with interleukin-1beta (IL-1beta). Although H(2)S by itself showed no effect on NO production, it augmented IL-beta-induced NO production and this effect was associated with increased expression of inducible NO synthase (iNOS) and activation of nuclear factor (NF)-kappaB. IL-1Beta activated the extracellular signal-regulated kinase 1/2 (ERK1/2), and this activation was also enhanced by H(2)S. Inhibition of ERK1/2 activation by the selective inhibitor U0126 inhibited IL-1beta-induced NF-kappaB activation, iNOS expression, and NO production either in the absence or presence of H(2)S. Our findings suggest that H(2)S enhances NO production and iNOS expression by potentiating IL-1beta-induced NF-kappaB activation through a mechanism involving ERK1/2 signaling cascade in rat VSMCs.

Find it online