MsrA protects cardiac myocytes against hypoxia/reoxygenation induced cell death

H. M. Prentice, I. A. Moench, Z. T. Rickaway, C. J. Dougherty, K. A. Webster, H. Weissbach

Research output: Contribution to journalArticlepeer-review

45 Scopus citations


Reactive oxygen species (ROS) are critical in tissue responses to ischemia-reperfusion. The enzyme methionine sulfoxide reductase-A (MsrA) is capable of protecting cells against oxidative damage by reversing damage to proteins caused by methionine oxidation or by decreasing ROS through a scavenger mechanism. The current study employed adenovirus mediated over-expression of MsrA in primary neonatal rat cardiac myocytes to determine the effect of this enzyme in protecting against hypoxia/reoxygenation in this tissue. Cells were transduced with MsrA encoding adenovirus and subjected to hypoxia/reoxygenation. Apoptotic cell death was decreased by greater than 45% in cells over-expressing MsrA relative to cells transduced with a control virus. Likewise total cell death as determined by levels of LDH release was dramatically decreased by MsrA over-expression. These observations indicate that MsrA is protective against hypoxia/reoxygenation stress in cardiac myocytes and point to MsrA as an important therapeutic target for ischemic heart disease.

Original languageEnglish (US)
Pages (from-to)775-778
Number of pages4
JournalBiochemical and biophysical research communications
Issue number3
StatePublished - Feb 15 2008


  • Hypoxia
  • Ischemia
  • Methionine sulfoxide reductase
  • Myocardium
  • Reactive oxygen species
  • ROS

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology


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