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• W147887029 abstract "Background Nitrite has been demonstrated to confer potent cardioprotection in animal models of acute myocardial infarction. Notably, administration of exogenous nitrite or elevations in endogenous nitrite during ischemia, or hours to days prior to the ischemic episode, significantly decrease infarct size after ischemia/reperfusion (I/R). When present during ischemia, the reduction of nitrite to bioactive NO by deoxygenated heme proteins accounts for its protective effects. However, the mechanism underlying normoxic nitrite-induced ischemic tolerance remains unexplored. Methods We established an in vitro cell model of hypoxia/reoxygenation (H/R) using H9c2 cardiomyocytes. Cells were treated with nitrite (10–100 μM; 30 min; 21% O 2 ), after which nitrite was removed, and cells incubated in normoxia for 5 min to 72 h prior to initiation of an ischemic episode (1% O 2 , pH 6.2) and reperfusion. Results Transient (30 min) normoxic nitrite treatment significantly attenuated cell death after H/R initiated 5 min–72 h later. Mechanistically, nitrite-mediated cytoprotection was dependent on increased activity of protein kinase A (PKA; 157.8 ± 23.8% of control), which propagated mitochondrial fusion through the phosphorylation and inhibition of dynamin related protein 1 (Drp1). This morphological change in mitochondrial phenotype led to a functional change characterized by a slight increase in mitochondrial superoxide generation (157.2 ± 16.3% of control). We show that this superoxide generated is responsible for the oxidation and subsequent activation of the cardioprotective mediator AMP kinase (214.7 ± 28.8% of control), as scavenging of reactive oxygen species by the mitochondrially targeted scavenger mitoTEMPO significantly abrogated AMPK activation and cytoprotection after H/R. Ongoing studies are investigating the mechanism by which nitrite modulates PKA activity. Preliminary data suggest that nitrite signaling may be mediated through the G protein beta 2 receptor (G β 2), as nitrite-induced phosphorylation of Drp1 was attenuated in the presence of the selective G β 2 inhibitor, ICI 118,551. Conclusions These data are the first to elucidate a mechanism by which nitrite confers ischemic resilience priorto I/R and are the first to report normoxic NO 2 - dependent activation of PKA and regulation of mitochondrial dynamics. Disclosure This work was supported by the Institute of Transfusion Medicine and the Hemophilia Center of Western Pennsylvania, the NIH (1R01HL096973 to SS; R01NS065789 to CTC) and by the American Heart Association (09SDG2150066 to SS)." @default.
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• W147887029 date "2013-04-01" @default.
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• W147887029 title "P43" @default.
• W147887029 doi "https://doi.org/10.1016/j.niox.2013.02.045" @default.
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