Estrogen induces cardioprotection in male C57BL/6J mice after acute myocardial infarction via decreased activity of matrix metalloproteinase-9 and increased Akt-Bcl-2 anti-apoptotic signaling

Int J Mol Med. 2011 Aug;28(2):231-7. doi: 10.3892/ijmm.2011.681. Epub 2011 Apr 20.

Abstract

In general, young men have a greater risk than age-matched women for many types of cardiovascular diseases, including ischemic heart diseases, such as acute or chronic myocardial infarction (MI)-induced heart failure. The effects of estrogen-replacement therapy in men have not been extensively studied. We evaluated the cardioprotective effects of supplemental estrogen against left anterior descending coronary ligation-induced MI in male C57BL/6J mice. A significantly lower prevalence of cardiac rupture was observed in estrogen-treated mice regardless of castration status. A reduced prevalence of cardiac rupture was associated with decreased activities of matrix metalloproteinase 9 (MMP-9) and increased expression of the anti-apoptotic gene Bcl-2. In vitro studies using H9C2 cells under simulated ischemia re-oxygenation treatment further support the role of estrogen receptor β in estrogen-mediated cardioprotection through the Akt-Bcl-2 signaling pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Cell Line, Tumor
  • Enzyme Activation / drug effects
  • Estrogens / pharmacology*
  • Heart Rupture, Post-Infarction / etiology
  • Humans
  • Male
  • Matrix Metalloproteinase 9 / metabolism*
  • Mice
  • Mice, Inbred C57BL
  • Myocardial Infarction / complications
  • Myocardial Infarction / metabolism*
  • Myocytes, Cardiac / drug effects
  • Myocytes, Cardiac / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Signal Transduction / drug effects*

Substances

  • Estrogens
  • Proto-Oncogene Proteins c-bcl-2
  • Proto-Oncogene Proteins c-akt
  • Matrix Metalloproteinase 9