Hydrogen sulfide mitigates cardiac remodeling during myocardial infarction via improvement of angiogenesis

Natia Qipshidze, Naira Metreveli, Paras Kumar Mishra, David Lominadze, Suresh C. Tyagi

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

Exogenous hydrogen sulfide (H2S) leads to down-regulation of inflammatory responses and provides myocardial protection during acute ischemia/reperfusion injury; however its role during chronic heart failure (CHF) due to myocardial infarction (MI) is yet to be unveiled. We previously reported that H2S inhibits antiangiogenic factors such, as endostatin and angiostatin, but a little is known about its effect on parstatin (a fragment of proteinase-activated receptor-1, PAR-1). We hypothesize that H2S inhibits parstatin formation and promotes VEGF activation, thus promoting angiogenesis and significantly limiting the extent of MI injury. To verify this hypothesis MI was created in 12 week-old male mice by ligation of left anterior descending artery (LAD). Sham surgery was performed except LAD ligation. After the surgery mice were treated with sodium hydrogen sulfide (30 μmol/l NaHS, a donor for H2S, in drinking water) for 4 weeks. The LV tissue was analyzed for VEGF, flk-1 and flt-1, endostatin, angiostatin and parstatin. The expression of VEGF, flk-1 and flt-1 were significantly increased in treated mice while the level of endostatin, angiostatin and parstatin were decreased compared to in untreated mice. The echocardiography in mice treated with H2S showed the improvement of heart function compared to in untreated mice. The X-ray and Doppler blood flow measurements showed enhancement of cardiac-angiogenesis in mice treated with H2S. This observed cytoprotection was associated with an inhibition of anti-angiogenic proteins and stimulation of angiogenic factors. We established that administration of H2S at the time of MI ameliorated infarct size and preserved LV function during development of MI in mice. These results suggest that H2S is cytoprotective and angioprotective during evolution of MI.

Original languageEnglish (US)
Pages (from-to)430-441
Number of pages12
JournalInternational Journal of Biological Sciences
Volume8
Issue number4
DOIs
StatePublished - Feb 28 2012
Externally publishedYes

Fingerprint

Hydrogen Sulfide
hydrogen sulfide
myocardial infarction
angiogenesis
Myocardial Infarction
Angiostatins
flow measurement
mice
Endostatins
blood
drinking water
sodium
Vascular Endothelial Growth Factor A
protein
arteries
Ligation
sodium sulfide
Arteries
surgery
Angiogenic Proteins

Keywords

  • Angiostatin
  • Endostatin
  • Hydrogen sulfide
  • Parstatin myocardial infarction
  • VEGF
  • flk-1
  • flt-1

ASJC Scopus subject areas

  • Ecology, Evolution, Behavior and Systematics
  • Applied Microbiology and Biotechnology
  • Molecular Biology
  • Developmental Biology
  • Cell Biology

Cite this

Hydrogen sulfide mitigates cardiac remodeling during myocardial infarction via improvement of angiogenesis. / Qipshidze, Natia; Metreveli, Naira; Mishra, Paras Kumar; Lominadze, David; Tyagi, Suresh C.

In: International Journal of Biological Sciences, Vol. 8, No. 4, 28.02.2012, p. 430-441.

Research output: Contribution to journalArticle

Qipshidze, Natia ; Metreveli, Naira ; Mishra, Paras Kumar ; Lominadze, David ; Tyagi, Suresh C. / Hydrogen sulfide mitigates cardiac remodeling during myocardial infarction via improvement of angiogenesis. In: International Journal of Biological Sciences. 2012 ; Vol. 8, No. 4. pp. 430-441.
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