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Fig. 4. CO activation of cardiac p38 MAP kinase and PI3-K/Akt. (A, top) Western blot of phosphorylated p38 (P-p38) in Wt and eNOS^–/– mice after treatment with CO (1250 ppm, 1 hour) with or without p38 inhibition (SB20). (Middle) Graphs indicate time courses for PGC-1, NRF1 and Tfam mRNA expression by real-time RT-PCR in Wt and eNOS^–/– mice after treatment with CO with or without the p38 inhibitor (SB20) Values are the mean ± s.e. normalized to GAPDH multiplied by total RNA mg/wet weight (^*P< 0.05 Wt vs eNOS^–/–). Inhibition of p38 did not attenuate the CO effect in either strain. (Bottom) Gel showing cardiac mtDNA copy number by competitive PCR in Wt and eNOS^–/– mice 24 hours after treatment with CO. The top band corresponds to the 571 bp of target mtDNA and the bottom band to the 332 bp DNA fragment. p38 inhibition did not alter the copy number. (B, top) Western blot of unphosphorylated Akt and phosphorylated Akt (pAkt) demonstrating an increase in the ratio of pAkt:Akt in Wt and eNOS^–/– mice after treatment with CO. (Middle) Western blot of cardiac unphosphorylated Bad and phosphorylated Bad (pBAD), showing the pBad:Bad ratio in Wt and eNOS^–/– mice after treatment with CO demonstrating phosphorylation of the mitochondrial anti-apoptotic protein. (Bottom) Western blot of Akt and pAkt showing the pAkt:Akt ratio in Wt heart after treatment with CO with or without hyperbaric oxygen (HBO), hypoxia (HH) or the p38 inhibitor (SB203580). Akt phosphorylation was not caused by hypoxia, and was prevented by hyperbaric oxygen but not by p38 inhibition (n=3).

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