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Papers In Press, published online ahead of print October 3, 2002
Institute for Arteriosclerosis Research, University of Munster, Munster 48149
Corresponding Author: seedorfu{at}uni-muenster.de
Clinical observations in patients with peroxisomal disorders and studies employing corresponding mouse models have shown that supra-physiological concentrations of dietary branched chain fatty acids (BCFAs) are associated with a high level of toxicity which is poorly understood at present. Here we show that phytanic and pristanic acid, two BCFAs that are metabolized in peroxisomes, promote apoptosis in cultured vascular smooth muscle cells of human, rat and porcine origin. Under the conditions used, the apoptosis promoting effect of BCFAs was neither shared by saturated or unsaturated straight-chain fatty acids nor by artificial peroxisome proliferators which, like phytanic and pristanic acid, have been shown to activate the peroxisome proliferator-activated receptor alpha (PPARalpha). We could demonstrate, however, that BCFA induce tumor necrosis factor alpha (TNFalpha) activation and secretion which is an obligatory step required for induction of apoptosis by BCFAs. Furthermore, incubation of VSMCs with BCFA increased inducible nitric oxide synthase (iNOS) mRNA and protein concentrations markedly within 2h of treatment. Correspondingly, apoptosis was significantly reduced when the cells were co-treated with the competitive NOS inhibitors monomethyl-L-arginine monoacetate and aminoguanidine. Moreover, co-incubation with TGFbeta1, previously shown to destabilize iNOS mRNA, also abolished apoptosis. These results establish a new signaling cascade in which natural BCFA induce NO-dependent apoptosis which is apparently triggered by autocrine secretion of TNFalpha in cultured VSMCs.
J. Biol. Chem, 10.1074/jbc.M204639200
Submitted on May 13, 2002
Revised on September 17, 2002
Accepted on October 3, 2002
Branched-chain fatty acids induce nitric oxide-dependent apoptosis in vascular smooth muscle cells
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