Vascular Endothelium Expresses 3-Mercaptopyruvate Sulfurtransferase and Produces Hydrogen Sulfide

Shibuya, Norihiro; Mikami, Yuzuru; Kimura, Yoshinobu; Nagahara, Noriyuki; Kimura, Hideo

doi:10.1093/jb/mvp111

Cited by 430 publications

(354 citation statements)

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“…R ecent evidence from CSE knockout mice suggests that loss of CSE gene expression results in a decrease in H 2 S production and a subsequent rise in blood pressure [16] . Furthermore, Shibuya et al and Olson et al showed that CSE, CBS, and 3MST were the three important H 2 S generating enzymes [13,14] . In our study, we found that the mRNA expression of 3MST in rat aorta was lower than that in the pulmonary artery, whereas the CSE protein was higher in the rat aorta than in the pulmonary artery.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have shown that cystathinonine gamma-lyase (CSE), cystathionine beta synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3MST) are three H 2 S generating enzymes [13][14] . It is shown that H 2 S relaxes blood vessels and lowers blood pressure by opening ATP-sensitive K + channels in vascular smooth muscle cells [15] .…”

Section: Wwwchinapharcom Sun Y Et Almentioning

confidence: 99%

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The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

et al. 2011

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Aim:To compare the vasorelaxing effects of hydrogen sulfide (H 2 S) on isolated aortic and pulmonary artery rings and to determine their action mechanisms. Methods: H 2 S-induced vasorelaxation of isolated rat aortic versus pulmonary artery rings under 95% O 2 and 5% CO 2 was analyzed. The expression of cystathinonine gamma-lyase (CSE), cystathionine beta synthase (CBS), 3-mercaptopyruvate sulfurtransferase (3MST), SUR2B and Kir6.1 was examined. Results: NaHS caused vasorelaxation of rat aortic and pulmonary artery rings in a dose-dependent manner. NaHS dilated aortic rings to a greater extent (16.4%, 38.4%, 64.1%, 84.3%, and 95.9% at concentrations of 50, 100, 200, 500, and 1000 μmol/L, respectively) than pulmonary artery rings (10.1%, 22.2%, 50.6%, 73.6%, and 84.6% at concentrations of 50, 100, 200, 500 and 1000 μmol/L, respec tively). The EC 50 of the vasorelaxant effect for aortic rings was 152.17 μmol/L, whereas the EC 50 for pulmonary artery rings was 233.65 μmol/L. The vasorelaxing effect of H 2 S was markedly blocked b y cellular and mitochondrial membrane K ATP channel blockers in aortic rings (P<0.01). In contrast, only the cellular membrane K ATP channel blocker inhibited H 2 S-induced vasorelaxation in pulmonary artery rings. SUR2B mRNA and protein expression was higher in aortic rings than in pulmonary artery rings. Cystathinonine gamma-lyase (CSE) but not cystathionine beta synthase (CBS) expression in aortic rings was higher than in pulmonary artery rings. 3-Mercapto pyruvate sulfurtransferase (3MST) mRNA was lower in aortic rings than in pulmonary artery rings. Conclusion: The vasorelaxing effect of H 2 S on isolated aortic rings was more pronounced than the effect on pulmonary artery rings at specific concentrations, which might be associated with increased expression of the K ATP channel subunit SUR2B.

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Section: Discussionmentioning

confidence: 99%

Section: Wwwchinapharcom Sun Y Et Almentioning

confidence: 99%

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

et al. 2011

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“…3-MST/CAT is localized in thoracic aorta ECs and produces H 2 S [13]; however, a vascular effect of 3-MST/CATderived H 2 S is unknown. Endogenous intra mitochondrial 3-MSTderived H 2 S has been shown to protect mitochondrial function/ metabolism [14].…”

Section: Introductionmentioning

confidence: 99%

H2S in the Vasculature: Controversy of Mechanisms in Physiology, Pathology and Beyond

Beyer¹

2015

Cardiol Pharmacol

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Hydrogen sulfide (H 2 S) is an endogenously gaseous messenger with a number of physiological effects. Pharmacological and genetic models point toward an important role for this vasodilator gas in the regulation of vascular tone, cardiac response to ischemia/reperfusion injury, and inflammation among others. Understanding the complex interaction of H 2 S with basic cellular signaling and its impact on endothelial and smooth muscle physiology may provide insights into the early stages of developing vascular inflammation and atherosclerosis or related vascular pathologies. The underlying mechanism of action is not completely understood. Recent evidence suggests a key role of H 2 S in protecting mitochondria against oxidative damage, regulation of ion channels and modulation of eNOS activity. This review will focus on the key role of H 2 S in the regulation of vascular function including free radical production and its physiological role in health and disease.

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“…Physiologically, H 2 S is generated from L-cysteine in reactions catalysed by three enzymes, including cystathionine-g-lyase(CSE), cystathionine-bsynthase(CBS) 1,2 and 3-mercap-topyruvatesulphurtransferase (3MST) 3 . Both CBS and CSE are localized to the cytoplasm, whereas 3MST is localized predominantly to the mitochondria.…”

mentioning

confidence: 99%

“…CSE is primarily responsible for most of the H 2 S production in the vasculature 4,5 , whereas CBS may be primarily responsible for H 2 S formation in the brain. H 2 S produced by 3MST regulates mitochondrial reactive oxygen species (ROS) production 3 . Intriguingly, the expression of H 2 S-generating enzymes and the endogenous production of H 2 S have recently been identified in male and female reproductive systems in several mammalian species [6][7][8][9][10][11] .…”

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confidence: 99%

Dysregulation of hydrogen sulphide metabolism impairs oviductal transport of embryos

Ning

Zhu

et al. 2014

Nat Commun

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Embryo retention in the fallopian tube is thought to lead to ectopic pregnancy, which is a significant cause of morbidity. Hydrogen sulphide (H 2 S) is a gaseotransmitter produced mainly by cystathionine-g-lyase and cystathionine-b-synthase. Here we show that cystathionine-g-lyase and cystathionine -b-synthase are ubiquitously distributed in human fallopian tube epithelium and that H 2 S signalling relaxes the spontaneous contraction of the human oviduct. Furthermore, an aberration in H 2 S signalling, either silenced or enhanced activity induced by pharmacologic or genetic methods, causes embryo retention and developmental delay in the mouse oviduct, which is partly reversed by administration of either GYY4137, a slow-releasing H 2 S donor, or NaHS. Our findings reveal a new regulatory mechanism for oviductal embryo transport.

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Vascular Endothelium Expresses 3-Mercaptopyruvate Sulfurtransferase and Produces Hydrogen Sulfide

Cited by 430 publications

References 23 publications

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

The vasorelaxing effect of hydrogen sulfide on isolated rat aortic rings versus pulmonary artery rings

H2S in the Vasculature: Controversy of Mechanisms in Physiology, Pathology and Beyond

Dysregulation of hydrogen sulphide metabolism impairs oviductal transport of embryos

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