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. 2014 Oct;86(4):450–462. doi: 10.1124/mol.114.094318

Fig. 4.

Fig. 4.

β-adrenoceptor/cAMP/PKA signaling regulates PARP activation in U937 cells during oxidative stress. The β-adrenoceptor antagonists propranolol (PP) (A), the adenylyl cyclase inhibitor DDA (B), or the PKA inhibitor PKAi (C) decrease cellular PARylation in U937 cells treated with H2O2. The β-adrenoceptor agonist isoproterenol (ISP) (D), the adenylyl-cyclase activator FSK (E), and the PKA activator 8Br-cAMP (F) enhance cellular PARylation during oxidative stress. The Western blot shown includes three separate technical replicates (lanes) for each experimental condition. Densitometric analysis of PARylation in H2O2-treated cells was set as 100% and effect of pharmacological modulators is presented as mean ± S.E.M. of three independent experiments; *P < 0.05.