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12,14-prostaglandin J2 increase mitochondrial complex I activity in endothelial cells
1 Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA
2 Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA; Center for Free Radical Biology, University of Alabama, Birmingham, AL, USA
* To whom correspondence should be addressed. E-mail: darley{at}path.uab.edu.
Oxidized lipids are capable of initiating diverse cellular responses through both receptor mediated mechanisms and direct post-translational modification of proteins. Oxidized lipids are capable of initiating diverse cellular responses through both receptor mediated mechanisms and direct post-translational modification of proteins. Typically exposure of cells to low concentrations of oxidized lipids induces cytoprotective pathways whereas high concentrations result in apoptosis. Interestingly, mitochondria can contribute to processes that result in either cytoprotection or cell death. The role of antioxidant defenses such as glutathione in adaptation to stress has been established but the potential interaction with mitochondrial function is unknown and is examined in this paper. HUVEC (human umbilical vein endothelial cells) were exposed to oxidized low density lipoprotein (oxLDL) or the electrophilic cyclopentenone, 15-Deoxy-
12,14-prostaglandin J2 (15d-PGJ2). We demonstrate that complex I activity, but not citrate synthase or cytochrome c oxidase, is significantly induced by oxLDL and 15d-PGJ2. The mechanism is not clear at present, but is independent of the induction of GSH PPAR-
and PPAR-
. This response is dependent on the induction of oxidative stress in the cells since it can be prevented by NO, probucol and the SOD mimetic, MnTBAP. This increased complex I activity appears to contribute to protection against apoptosis induced by 4-hydroxynonenal.
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