期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 111, 期 8, 页码 3182-3187出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1321871111
关键词
eNOS uncoupling; myocardial infarction; cystathionase; Cth; nitrite
资金
- National Heart, Lung, and Blood Institute [1R01 HL092141, 1R01 HL093579, 1U24 HL 094373, 1P20 HL113452, 5R01 HL 098481]
- Canadian Institutes of Health Research
- Carlyle Fraser Heart Center of Emory University
- Louisiana State University Health Foundation in New Orleans
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.
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