Hydrogen sulfide potentiates interleukin-1{beta}-induced nitric oxide production via enhancement of extracellular signal-regulated kinase activation in rat vascular smooth muscle cells
- Medicinal Resources Research Institute, Wonkwang University, Department of Microbiology and Immunology, Wonkwang University School of Medicine, Chonbug 570-749 (Korea, Republic of)
- Department of Pharmacology, Wonkwang University School of Medicine, Chonbug 570-749 (Korea, Republic of)
- Department of Urology, College of Medicine, Kosin University, Busan 602-702 (Korea, Republic of)
- Division of Biological Science, College of Natural Science, Chonbuk National University, Chonbug 570-756 (Korea, Republic of)
Hydrogen sulfide (H{sub 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{sub 2}S could affect NO production in rat vascular smooth muscle cells (VSMCs) stimulated with interleukin-1{beta} (IL-1{beta}). Although H{sub 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)-{kappa}B. IL-1{beta} activated the extracellular signal-regulated kinase 1/2 (ERK1/2), and this activation was also enhanced by H{sub 2}S. Inhibition of ERK1/2 activation by the selective inhibitor U0126 inhibited IL-1{beta}-induced NF-{kappa}B activation, iNOS expression, and NO production either in the absence or presence of H{sub 2}S. Our findings suggest that H{sub 2}S enhances NO production and iNOS expression by potentiating IL-1{beta}-induced NF-{kappa}B activation through a mechanism involving ERK1/2 signaling cascade in rat VSMCs.
- OSTI ID:
- 20854334
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 345, Issue 3; Other Information: DOI: 10.1016/j.bbrc.2006.05.002; PII: S0006-291X(06)01019-9; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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