Stable transfection of UCP1 confers resistance to hypoxia/reoxygenation in a heart-derived cell line.
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.
Bienengraeber
Martin
M
Division of Cardiovascular Diseases, Departments of Medicine, Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Mayo Foundation, Guggenheim-7F, Rochester, MN 55905, USA.
Ozcan
Cevher
C
Terzic
Andre
A
D002352:Carrier Proteins / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000378:metabolism*; D007473:Ion Channels; D008565:Membrane Proteins / Q000235:genetics* / Q000378:metabolism; D008928:Mitochondria; D024101:Mitochondrial Proteins; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000378:metabolism*; D014162:Transfection; D000071256:Uncoupling Protein 1
D002352:Carrier Proteins; D007473:Ion Channels; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; C000604371:UCP1 protein, human; D000071256:Uncoupling Protein 1