Idioma:

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

King, Adrienne L. ; Polhemus, David J. ; Bhushan, Shashi ; Otsuka, Hiroyuki ; Kondo, Kazuhisa ; Nicholson, Chad K. ; Bradley, Jessica M. ; Islam, Kazi N. ; Calvert, John W. ; Tao, Ya-Xiong ; Dugas, Tammy R. ; Kelley, Eric E. ; Elrod, John W. ; Huang, Paul L. ; Wang, Rui ; Lefer, David J.

Proceedings of the National Academy of Sciences - PNAS, 2014-02, Vol.111 (8), p.3182-3187 [Periódico revisado por pares]

United States: National Academy of Sciences

Texto completo disponível

Citações Citado por

Enviar para

Título:
Hydrogen sulfide cytoprotective signaling is endothelial nitric oxide synthase-nitric oxide dependent
Autor: King, Adrienne L. ; Polhemus, David J. ; Bhushan, Shashi ; Otsuka, Hiroyuki ; Kondo, Kazuhisa ; Nicholson, Chad K. ; Bradley, Jessica M. ; Islam, Kazi N. ; Calvert, John W. ; Tao, Ya-Xiong ; Dugas, Tammy R. ; Kelley, Eric E. ; Elrod, John W. ; Huang, Paul L. ; Wang, Rui ; Lefer, David J.
Assuntos: Alanine Transaminase - blood ; Analysis of Variance ; Animals ; Aspartate Aminotransferases - blood ; Bioavailability ; Biological Sciences ; Blotting, Western ; Cardiovascular disease ; Chromatography, High Pressure Liquid ; Cystathionine gamma-Lyase - genetics ; Cytoprotection - drug effects ; Cytoprotection - physiology ; Enzymes ; Heart ; Hydrogen ; Hydrogen sulfide ; Hydrogen Sulfide - metabolism ; Hydrogen Sulfide - pharmacology ; Immunohistochemistry ; Liver ; Mice ; Mice, Knockout ; Mitochondria - physiology ; Myocardial Reperfusion Injury - drug therapy ; Myocardial Reperfusion Injury - metabolism ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type III - metabolism ; Nitrites ; Oxidative stress ; Oxidative Stress - physiology ; Oxides ; Oxygen Consumption - physiology ; Phosphorylation ; Physical trauma ; Rodents ; Signal transduction ; Signal Transduction - physiology ; Sulfides ; Troponin I - metabolism
É parte de: Proceedings of the National Academy of Sciences - PNAS, 2014-02, Vol.111 (8), p.3182-3187
Notas: http://dx.doi.org/10.1073/pnas.1321871111
Author contributions: D.J.P., K.K., E.E.K., J.W.E., and D.J.L. designed research; A.L.K., D.J.P., S.B., H.O., K.K., C.K.N., K.N.I., Y.-X.T., T.R.D., E.E.K., and J.W.E. performed research; J.W.C., Y.-X.T., T.R.D., E.E.K., P.L.H., and R.W. contributed new reagents/analytic tools; A.L.K. and D.J.P. analyzed data; and D.J.P., J.M.B., and D.J.L. wrote the paper.
Edited by Louis J. Ignarro, UCLA School of Medicine, Beverly Hills, CA, and approved January 15, 2014 (received for review November 21, 2013)
1A.L.K. and D.J.P. contributed equally to this work.
Descrição: Previous studies have demonstrated that hydrogen sulfide (H ₂S) protects against multiple cardiovascular disease states in a similar manner as nitric oxide (NO). H ₂S therapy also has been shown to augment NO bioavailability and signaling. The purpose of this study was to investigate the impact of H ₂S deficiency on endothelial NO synthase (eNOS) function, NO production, and ischemia/reperfusion (I/R) injury. We found that mice lacking the H ₂S-producing enzyme cystathionine γ-lyase (CSE) exhibit elevated oxidative stress, dysfunctional eNOS, diminished NO levels, and exacerbated myocardial and hepatic I/R injury. In CSE KO mice, acute H ₂S therapy restored eNOS function and NO bioavailability and attenuated I/R injury. In addition, we found that H ₂S therapy fails to protect against I/R in eNOS phosphomutant mice (S1179A). Our results suggest that H ₂S-mediated cytoprotective signaling in the setting of I/R injury is dependent in large part on eNOS activation and NO generation.
Editor: United States: National Academy of Sciences
Idioma: Inglês

Links

View this record in MEDLINE/PubMed

Voltar para lista de resultados

Realização: Logos de Redes Sociais:

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

King, Adrienne L. ; Polhemus, David J. ; Bhushan, Shashi ; Otsuka, Hiroyuki ; Kondo, Kazuhisa ; Nicholson, Chad K. ; Bradley, Jessica M. ; Islam, Kazi N. ; Calvert, John W. ; Tao, Ya-Xiong ; Dugas, Tammy R. ; Kelley, Eric E. ; Elrod, John W. ; Huang, Paul L. ; Wang, Rui ; Lefer, David J.

United States: National Academy of Sciences

Buscando em bases de dados remotas. Favor aguardar.