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Published online before print August 4, 2006 as doi: 10.1096/fj.05-5189fje.

Nitric oxide regulates mitochondrial oxidative stress protection via the transcriptional coactivator PGC-1{alpha}

Sara Borniquel, Inmaculada Valle, Susana Cadenas, Santiago Lamas, and María Monsalve

E-mail contact: mmonsalve@cnic.es

Nitric oxide (NO) has both prooxidant and antioxidant activities in the endothelium; however, the molecular mechanisms involved are still a matter of controversy. PGC-1{alpha} [peroxisome proliferators-activated receptor (PPAR) {gamma} coactivator 1-{alpha}] induces the expression of several members of the mitochondrial reactive oxygen species (ROS) detoxification system. Here, we show that NO regulates this system through the modulation of PGC-1{alpha} expression. Short-term (<12 h) treatment of endothelial cells with NO donors down-regulates PGC-1{alpha} expression, whereas long-term (>24 h) treatment up-regulates it. Treatment with the NOS inhibitor L-NAME has the opposite effect. Down-regulation of PGC-1{alpha} by NO is mediated by protein kinase G (PKG). It is blocked by the soluble guanylate cyclase (sGC) inhibitor ODQ and the PKG inhibitor KT5823, and mimicked by the cGMP analog 8-Br-cGMP. Changes in PGC-1{alpha} expression are in all cases paralleled by corresponding variations in the mitochondrial ROS detoxification system. Cells that transiently overexpress PGC-1{alpha} from the cytomeglovirus (CMV) promoter respond poorly to NO donors. Analysis of tissues from eNOS-/- mice showed reduced levels of PGC-1{alpha} and the mitochondrial ROS detoxification system. These data suggest that NO can regulate the mitochondrial ROS detoxification system both positively and negatively through PGC-1{alpha}. --Borniquel, S., Valle, I., Cadenas, S., Lamas, S., and Monsalve, M. Nitric oxide regulates mitochondrial oxidative stress protection via the transcriptional coactivator PGC-1{alpha}.




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