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      Hydrogen sulfide inhibits the calcification and osteoblastic differentiation of vascular smooth muscle cells

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          Abstract

          Osteoblastic differentiation of vascular smooth muscle cells (VSMCs) is involved in the pathogenesis of vascular calcification. Hydrogen sulfide (H 2S) is a gas endogenously produced by cystathionine γ-lyase in VSMC. Here we determined whether H 2S plays a role in phosphate-induced osteoblastic transformation and mineralization of VSMC. Hydrogen sulfide was found to inhibit calcium deposition in the extracellular matrix and to suppress the induction of the genes involved in osteoblastic transformation of VSMC: alkaline phosphatase, osteocalcin, and Cbfa1. Moreover, phosphate uptake and phosphate-triggered upregulation of the sodium-dependent phosphate cotransporter (Pit-1) were also prevented by H 2S. Reduction of endogenous production of H 2S by inhibition of cystathionine γ-lyase activity resulted in increased osteoblastic transformation and mineralization. Low plasma levels of H 2S, associated with decreased cystathionine γ-lyase enzyme activity, were found in patients with chronic kidney disease receiving hemodialysis. Thus, H 2S is a potent inhibitor of phosphate-induced calcification and osteoblastic differentiation of VSMC. This mechanism might contribute to accelerated vascular calcification in chronic kidney disease.

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          H2S as a physiologic vasorelaxant: hypertension in mice with deletion of cystathionine gamma-lyase.

          Guangdong Yang, Lingyun Wu, Bo Jiang … (2008)
          Studies of nitric oxide over the past two decades have highlighted the fundamental importance of gaseous signaling molecules in biology and medicine. The physiological role of other gases such as carbon monoxide and hydrogen sulfide (H2S) is now receiving increasing attention. Here we show that H2S is physiologically generated by cystathionine gamma-lyase (CSE) and that genetic deletion of this enzyme in mice markedly reduces H2S levels in the serum, heart, aorta, and other tissues. Mutant mice lacking CSE display pronounced hypertension and diminished endothelium-dependent vasorelaxation. CSE is physiologically activated by calcium-calmodulin, which is a mechanism for H2S formation in response to vascular activation. These findings provide direct evidence that H2S is a physiologic vasodilator and regulator of blood pressure.
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            Two's company, three's a crowd: can H2S be the third endogenous gaseous transmitter?

            Rui Wang (2002)
            Bearing the public image of a deadly "gas of rotten eggs," hydrogen sulfide (H2S) can be generated in many types of mammalian cells. Functionally, H2S has been implicated in the induction of hippocampal long-term potentiation, brain development, and blood pressure regulation. By acting specifically on KATP channels, H2S can hyperpolarize cell membranes, relax smooth muscle cells, or decrease neuronal excitability. The endogenous metabolism and physiological functions of H2S position this gas well in the novel family of endogenous gaseous transmitters, termed "gasotransmitters." It is hypothesized that H2S is the third endogenous signaling gasotransmitter, besides nitric oxide and carbon monoxide. This positioning of H2S will open an exciting field-H2S physiology-encompassing realization of the interaction of H2S and other gasotransmitters, sulfurating modification of proteins, and the functional role of H2S in multiple systems. It may shed light on the pathogenesis of many diseases related to the abnormal metabolism of H2S.
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              The vasorelaxant effect of H(2)S as a novel endogenous gaseous K(ATP) channel opener.

              W Zhao, J ZHANG, Y. Lu … (2001)
              Hydrogen sulfide (H(2)S) has been traditionally viewed as a toxic gas. It is also, however, endogenously generated from cysteine metabolism. We attempted to assess the physiological role of H(2)S in the regulation of vascular contractility, the modulation of H(2)S production in vascular tissues, and the underlying mechanisms. Intravenous bolus injection of H(2)S transiently decreased blood pressure of rats by 12- 30 mmHg, which was antagonized by prior blockade of K(ATP) channels. H(2)S relaxed rat aortic tissues in vitro in a K(ATP) channel-dependent manner. In isolated vascular smooth muscle cells (SMCs), H(2)S directly increased K(ATP) channel currents and hyperpolarized membrane. The expression of H(2)S-generating enzyme was identified in vascular SMCs, but not in endothelium. The endogenous production of H(2)S from different vascular tissues was also directly measured with the abundant level in the order of tail artery, aorta and mesenteric artery. Most importantly, H(2)S production from vascular tissues was enhanced by nitric oxide. Our results demonstrate that H(2)S is an important endogenous vasoactive factor and the first identified gaseous opener of K(ATP) channels in vascular SMCs.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Kidney Int
                Title: Kidney International
                Publisher: Nature Publishing Group
                ISSN (Print): 0085-2538
                ISSN (Electronic): 1523-1755
                Publication date (Print): October 2011
                Publication date (Electronic): 29 June 2011
                Volume: 80
                Issue: 7
                Pages: 731-739
                Affiliations
                [1 ]simpleHemostasis, Thrombosis and Vascular Biology Research Group, Hungarian Academy of Sciences , Debrecen, Hungary
                [2 ]simpleDivision of Nephrology, Department of Medicine, University of Debrecen , Debrecen, Hungary
                [3 ]simpleUniversity of Medicine and Pharmacy , Targu Mures, Romania
                [4 ]simpleDepartment of Medicine, Nephrology Research and Training Center and Center for Free Radical Biology, University of Alabama at Birmingham , Birmingham, Alabama, USA
                [5 ]simpleDepartment of Biochemistry and Molecular Biology, University of Debrecen , Debrecen, Hungary
                [6 ]simpleDepartment of Pediatrics, University of Debrecen , Debrecen, Hungary
                Author notes
                [* ]simpleDivision of Nephrology, Department of Medicine, Hemostasis, Thrombosis and Vascular Biology Research Group, Hungarian Academy of Sciences , Pf. 19, Nagyerdei krt. 98, Debrecen 4012, Hungary. E-mail: balla@ 123456internal.med.unideb.hu
                [7]

                These authors share last authorship.

                Article
                Publisher Item ID: ki2011212
                DOI: 10.1038/ki.2011.212
                PMC ID: 3257044
                PubMed ID: 21716261
                SO-VID: 6d4fbcfb-1511-4da7-9d23-21de65b87a51
                Copyright © Copyright © 2011 International Society of Nephrology
                License:

                This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

                History
                Date received : 19 August 2010
                Date revision received : 27 April 2011
                Date accepted : 10 May 2011
                Categories
                Subject: Original Article

                ScienceOpen disciplines: Nephrology
                Keywords: vascular smooth muscle cell,cystathionine γ-lyase,hydrogen sulfide,vascular calcification
                Data availability:
                ScienceOpen disciplines: Nephrology
                Keywords: vascular smooth muscle cell, cystathionine γ-lyase, hydrogen sulfide, vascular calcification

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