Paras Kumar Mishra, PhD

Associate Professor at University of Nebraska Medical Center


Curriculum vitae



Cellular and Integrative Physiology

University of Nebraska Medical Center



Hydrogen sulfide improves angiogenesis and regulates cardiac function and structure during myocardial infarction in mice


Journal article


Natia Qipshidze, P. Mishra, Naira S. Metreveli, D. Lominadze, Suresh Tyagi
2011

Semantic Scholar DOI
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APA   Click to copy
Qipshidze, N., Mishra, P., Metreveli, N. S., Lominadze, D., & Tyagi, S. (2011). Hydrogen sulfide improves angiogenesis and regulates cardiac function and structure during myocardial infarction in mice.


Chicago/Turabian   Click to copy
Qipshidze, Natia, P. Mishra, Naira S. Metreveli, D. Lominadze, and Suresh Tyagi. “Hydrogen Sulfide Improves Angiogenesis and Regulates Cardiac Function and Structure during Myocardial Infarction in Mice” (2011).


MLA   Click to copy
Qipshidze, Natia, et al. Hydrogen Sulfide Improves Angiogenesis and Regulates Cardiac Function and Structure during Myocardial Infarction in Mice. 2011.


BibTeX   Click to copy

@article{natia2011a,
  title = {Hydrogen sulfide improves angiogenesis and regulates cardiac function and structure during myocardial infarction in mice},
  year = {2011},
  author = {Qipshidze, Natia and Mishra, P. and Metreveli, Naira S. and Lominadze, D. and Tyagi, Suresh}
}

Abstract

Previously we showed that the homocysteine (Hcy) level was increased during the myocardial infarction (MI), which was caused by decreasing of Hcy lowering factors, cystathionine β‐synthase and cystathionine γ‐lyase (CGL). It is known that hydrogen sulfide (H2S) is a cardioprotective agent and decreases the level of Hcy in the heart. In the present study we tested its cardio protective potential during MI. MI was induced in 12‐week‐old mice by ligation of left anterior descending artery. Sham surgery was performed except the ligation. After the surgery, mice were given drinking water with or without sodium hydrosulfide (NaHS, H2S donor) for 4 weeks. Levels of VEGF, flk‐1 and flt‐1 were significantly increased and the expression of anti‐angiogenic proteins (endostatin, angiostatin, parstatin) were decreased in treated mice compared to the untreated, control group. The echocardiography showed improvement in heart function in treated mice compared to control group. This observed cytoprotection was associated with a downregulation of anti‐angiogenic proteins and stimulation of angiogenesis. In addition, we found that treatment with NaHS significantly increasef the level of CGL, which significantly lowered the damaged part. The present study demonstrates that H2S, through cytoprotection and angioprotection, ameliorates infarct size and preserves left ventricular function during MI.


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