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. 2019 Nov 1;317(6):H1231–H1242. doi: 10.1152/ajpheart.00237.2019

Fig. 2.

Fig. 2.

Oxidative stress alone induces type I cAMP-dependent protein kinase (PKA) regulatory α-subunit (RIα) downregulation in adult mouse ventricular myocytes (AMVMs). A: immunoblot analysis of AMVM cell cultures treated for 30 min with the oxidant H2O2 at the indicated micromolar concentrations. Opa1, optic atrophy protein 1; COXIV, cytochrome-c oxidase. B: quantification of RIα, catalytic subunit of PKA (PKAc), RIIα, and A-kinase anchoring protein 1 (AKAP1) expression from H2O2 dose-response experiments in A. Data are presented as means ± SD; n = 4–7 biological replicates. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001 compared with 0-µM treatment. C: immunoblot analysis of AMVM cell cultures treated with 100 μΜ H2O2 for the indicated time periods. D: quantification of RIα, PKAc, RIIα, and AKAP1 expression from 100 μM H2O2 time-course experiments from C. Data are presented as means ± SD; n = 3 biological replicates. *P < 0.05, **P < 0.01, and ***P < 0.001 compared with 0-min time point.