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. 2015 Jul 29;309(6):C425–C436. doi: 10.1152/ajpcell.00058.2015

Fig. 6.

Fig. 6.

Rp-adenosine 3′,5′-cyclic monophosphorothioate triethylammonium salt (Rp-cAMP) blocks the DBcAMP-induced actions in HL-1 cells. HL-1 cells were treated with vehicle [dimethyl sulfoxide (DMSO)], 100 μM Rp-cAMP (low), 250 μM Rp-cAMP (high), 1.5 mM DBcAMP, 1.5 mM DBcAMP + 100 μM Rp-cAMP (low), or 1 mM cAMP + 250 μM Rp-cAMP (high) for 48 h. Cell size analysis on phase-contrast images showed that Rp-cAMP blocked the DBcAMP-induced cardiomyocyte enlargement (A). Rp-cAMP also inhibited the upregulation of Myh6, Myh7, Myh7b, and troponin I type 3 (Tnni3) mRNA expression following DBcAMP treatment (B). Furthermore, Rp-cAMP normalized the expression of Dnmts mRNAs (C) as well as global DNA methylation levels in DBcAMP-treated cells (D). However, Rp-cAMP was unable to normalize the mRNA expression of B-type natriuretic peptide (Bnp) (B). Bars ± SE represent fold changes that are normalized to β-actin and relative to individual controls (n = 3, *P < 0.05, **P < 0.01, and ***P < 0.001 vs. vehicle; #P < 0.05, ##P < 0.01, and ###P < 0.001 vs. 1.5 mM DBcAMP group).