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ABSTRACT: Aims
Both mitochondria and nitric oxide (NO*) contribute to cardioprotection by ischaemic preconditioning (IPC). IPC causes mild uncoupling of mitochondria via uncoupling proteins (UCPs) and the adenine nucleotide translocase (ANT), and mild uncoupling per se is cardioprotective. Although electrophilic lipids are known to activate mitochondrial uncoupling, the role of such species in IPC-induced uncoupling and cardioprotection is unclear. We hypothesized that endogenous formation of NO*-derived electrophilic lipids (nitroalkenes such as nitro-linoleate, LNO2) during IPC may stimulate mitochondrial uncoupling via post-translational modification of UCPs and ANT, thus affording cardioprotection.Methods
Hearts from male Sprague-Dawley rats were Langendorff-perfused and subjecte
SUBMITTER: Nadtochiy SM
PROVIDER: S-EPMC2675927 | biostudies-literature | 2009 May
REPOSITORIES: biostudies-literature