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Hydrogen sulfide potentiates interleukin-1beta-induced nitric oxide production via enhancement of extracellular signal-regulated kinase activation in rat vascular smooth muscle cells.
Biochem Biophys Res Commun 2006; 345(3):938-44BB

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.

Authors+Show Affiliations

Medicinal Resources Research Institute, Wonkwang University, Department of Microbiology and Immunology, Wonkwang University School of Medicine, Chonbug 570-749, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16707097

Citation

Jeong, Sun-Oh, et al. "Hydrogen Sulfide Potentiates Interleukin-1beta-induced Nitric Oxide Production Via Enhancement of Extracellular Signal-regulated Kinase Activation in Rat Vascular Smooth Muscle Cells." Biochemical and Biophysical Research Communications, vol. 345, no. 3, 2006, pp. 938-44.
Jeong SO, Pae HO, Oh GS, et al. Hydrogen sulfide potentiates interleukin-1beta-induced nitric oxide production via enhancement of extracellular signal-regulated kinase activation in rat vascular smooth muscle cells. Biochem Biophys Res Commun. 2006;345(3):938-44.
Jeong, S. O., Pae, H. O., Oh, G. S., Jeong, G. S., Lee, B. S., Lee, S., ... Chung, H. T. (2006). Hydrogen sulfide potentiates interleukin-1beta-induced nitric oxide production via enhancement of extracellular signal-regulated kinase activation in rat vascular smooth muscle cells. Biochemical and Biophysical Research Communications, 345(3), pp. 938-44.
Jeong SO, et al. Hydrogen Sulfide Potentiates Interleukin-1beta-induced Nitric Oxide Production Via Enhancement of Extracellular Signal-regulated Kinase Activation in Rat Vascular Smooth Muscle Cells. Biochem Biophys Res Commun. 2006 Jul 7;345(3):938-44. PubMed PMID: 16707097.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hydrogen sulfide potentiates interleukin-1beta-induced nitric oxide production via enhancement of extracellular signal-regulated kinase activation in rat vascular smooth muscle cells. AU - Jeong,Sun-Oh, AU - Pae,Hyun-Ock, AU - Oh,Gi-Su, AU - Jeong,Gil-Saeng, AU - Lee,Bok-Soo, AU - Lee,Seoul, AU - Kim,Du Yong, AU - Rhew,Hyun Yul, AU - Lee,Kang-Min, AU - Chung,Hun-Taeg, Y1 - 2006/05/08/ PY - 2006/04/21/received PY - 2006/05/01/accepted PY - 2006/5/19/pubmed PY - 2006/8/2/medline PY - 2006/5/19/entrez SP - 938 EP - 44 JF - Biochemical and biophysical research communications JO - Biochem. Biophys. Res. Commun. VL - 345 IS - 3 N2 - 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. SN - 0006-291X UR - https://www.unboundmedicine.com/medline/citation/16707097/Hydrogen_sulfide_potentiates_interleukin_1beta_induced_nitric_oxide_production_via_enhancement_of_extracellular_signal_regulated_kinase_activation_in_rat_vascular_smooth_muscle_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(06)01019-9 DB - PRIME DP - Unbound Medicine ER -