Methionine sulfoxide reductase A (MsrA) protects cultured mouse embryonic stem cells from H2O2-mediated oxidative stress

Chi Zhang, Pingping Jia, Yuanyuan Jia, Herbert Weissbach, Keith A. Webster, Xupei Huang, Sharon L. Lemanski, Mohan Achary, Larry F. Lemanski

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

Methionine sulfoxide reductase A (MsrA), a member of the Msr gene family, can reduce methionine sulfoxide residues in proteins formed by oxidation of methionine by reactive oxygen species (ROS). Msr is an important protein repair system which can also function to scavenge ROS. Our studies have confirmed the expression of MsrA in mouse embryonic stem cells (ESCs) in culture conditions. A cytosol-located and mitochondria-enriched expression pattern has been observed in these cells. To confirm the protective function of MsrA in ESCs against oxidative stress, a siRNA approach has been used to knockdown MsrA expression in ES cells which showed less resistance than control cells to hydrogen peroxide treatment. Overexpression of MsrA gene products in ES cells showed improved survivability of these cells to hydrogen peroxide treatment. Our results indicate that MsrA plays an important role in cellular defenses against oxidative stress in ESCs. Msr genes may provide a new target in stem cells to increase their survivability during the therapeutic applications.

Original languageEnglish (US)
Pages (from-to)94-103
Number of pages10
JournalJournal of cellular biochemistry
Volume111
Issue number1
DOIs
StatePublished - Sep 1 2010

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Keywords

  • Anoxia/reoxygenation
  • Cell death
  • MsrA
  • siRNA

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Cite this

Zhang, C., Jia, P., Jia, Y., Weissbach, H., Webster, K. A., Huang, X., Lemanski, S. L., Achary, M., & Lemanski, L. F. (2010). Methionine sulfoxide reductase A (MsrA) protects cultured mouse embryonic stem cells from H2O2-mediated oxidative stress. Journal of cellular biochemistry, 111(1), 94-103. https://doi.org/10.1002/jcb.22666