Stable transfection of UCP1 confers resistance to hypoxia/reoxygenation in a heart-derived cell line

Martin Bienengraeber, Cevher Ozcan, Andre Terzic

Research output: Contribution to journalArticle

45 Scopus citations


Mitochondrial uncoupling proteins, which secure physiological uncoupling of oxidative phosphorylation, have been proposed to serve as an oxidative-stress compensatory mechanism. Here, heart-derived H9c2 cells acquired improved resistance to injury upon transfection of the prototypic uncoupling protein UCP1. Following hypoxia/reoxygenation, stable overexpression of UCP1 provided enhanced cardioblast survival with preserved mitochondrial structure and function, while limiting reactive oxygen species formation. Thus, transfection of mitochondrial UCP1 provides a strategy for generation of a stress-resistant cardiac cell phenotype.

Original languageEnglish (US)
Pages (from-to)861-865
Number of pages5
JournalJournal of Molecular and Cellular Cardiology
Issue number7
StatePublished - Jul 1 2003



  • Cardioprotection
  • Mitochondria
  • Reactive oxygen species
  • Uncoupling protein

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

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