Hydrogen sulfide cytoprotective signaling is endothelial nitric oxide synthase-nitric oxide dependent

被引：300

作者：

King, Adrienne L. ^{[1
,2
]}

Polhemus, David J. ^{[3
,4
]}

Bhushan, Shashi ^{[3
,4
]}

Otsuka, Hiroyuki ^{[3
,4
]}

Kondo, Kazuhisa ^{[1
,2
]}

Nicholson, Chad K. ^{[1
,2
]}

Bradley, Jessica M. ^{[3
,4
]}

Islam, Kazi N. ^{[3
,4
]}

Calvert, John W. ^{[1
,2
]}

Tao, Ya-Xiong ^{[5
]}

Dugas, Tammy R. ^{[6
]}

Kelley, Eric E. ^{[7
,8
]}

Elrod, John W. ^{[9
]}

Huang, Paul L. ^{[10
,11
]}

Wang, Rui ^{[12
]}

Lefer, David J. ^{[3
,4
]}

机构：

[1] Emory Univ, Sch Med, Dept Surg, Atlanta, GA 30308 USA

[2] Emory Univ, Sch Med, Carlyle Fraser Heart Ctr, Atlanta, GA 30308 USA

[3] Louisiana State Univ, Hlth Sci Ctr, Dept Pharmacol & Expt Therapeut, New Orleans, LA 70112 USA

[4] Louisiana State Univ, Hlth Sci Ctr, Cardiovasc Ctr Excellence, New Orleans, LA 70112 USA

[5] Auburn Univ, Coll Vet Med, Dept Anat Physiol & Pharmacol, Auburn, AL 36832 USA

[6] Louisiana State Univ, Hlth Sci Ctr Shreveport, Dept Pharmacol Toxicol & Neurosci, Shreveport, LA 71130 USA

[7] Univ Pittsburgh, Dept Anesthesiol, Pittsburgh, PA 15213 USA

[8] Univ Pittsburgh, Vasc Med Inst, Pittsburgh, PA 15213 USA

[9] Temple Univ, Dept Pharmacol, Ctr Translat Med, Philadelphia, PA 19140 USA

[10] Massachusetts Gen Hosp, Cardiovasc Res Ctr, Boston, MA 02114 USA

[11] Massachusetts Gen Hosp, Div Cardiol, Boston, MA 02114 USA

[12] Lakehead Univ, Dept Biol, Thunder Bay, ON P7B 5E1, Canada

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2014年 / 111卷 / 08期

基金：

加拿大健康研究院;

关键词：

eNOS uncoupling; myocardial infarction; cystathionase; Cth; nitrite; MYOCARDIAL ISCHEMIA-REPERFUSION; INDUCED HEART-FAILURE; MOUSE HEART; IN-VIVO; PROTECTS; INJURY; AKT; H2S; TETRAHYDROBIOPTERIN; PHOSPHORYLATION;

D O I：

10.1073/pnas.1321871111

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Previous studies have demonstrated that hydrogen sulfide (H2S) protects against multiple cardiovascular disease states in a similar manner as nitric oxide (NO). H2S therapy also has been shown to augment NO bioavailability and signaling. The purpose of this study was to investigate the impact of H2S deficiency on endothelial NO synthase (eNOS) function, NO production, and ischemia/reperfusion (I/R) injury. We found that mice lacking the H2S-producing enzyme cystathionine gamma-lyase (CSE) exhibit elevated oxidative stress, dysfunctional eNOS, diminished NO levels, and exacerbated myocardial and hepatic I/R injury. In CSE KO mice, acute H2S therapy restored eNOS function and NO bioavailability and attenuated I/R injury. In addition, we found that H2S therapy fails to protect against I/R in eNOS phosphomutant mice (S1179A). Our results suggest that H2S-mediated cytoprotective signaling in the setting of I/R injury is dependent in large part on eNOS activation and NO generation.

引用

页码：3182 / 3187

页数：6

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