Stable transfection of UCP1 confers resistance to hypoxia/reoxygenation in a heart-derived cell line. J Mol Cell Cardiol 2003 Jul;35(7):861-5
Date
06/24/2003Pubmed ID
12818577DOI
10.1016/s0022-2828(03)00147-0Scopus ID
2-s2.0-0038123011 (requires institutional sign-in at Scopus site) 55 CitationsAbstract
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.
Author List
Bienengraeber M, Ozcan C, Terzic AMESH terms used to index this publication - Major topics in bold
Carrier ProteinsHumans
Hypoxia
Ion Channels
Membrane Proteins
Mitochondria
Mitochondrial Proteins
Myocardial Reperfusion Injury
Myocytes, Cardiac
Transfection
Uncoupling Protein 1
