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. 2018 Jul 17;115(1):94–106. doi: 10.1093/cvr/cvy173

Figure 2.

Figure 2

Epac1-manipulation in vitro with and without profibrotic stimuli in isolated atrial fibroblasts. (A) Epac1-activation via 8-pCPT (50-μmol/L) significantly decreased collagen1A1 (COL1A1) and Epac1 inhibition with ESI-09 (1-μmol/L) upregulated COL1A1 mRNA-expression. (B) Representative immunoblots (top) and quantification (bottom) for collagen-I secretion. Immunoblots were performed on culture-supernatant after 48-h treatment with 8-pCPT or ESI-09. (C) Incubation with 10 ng/mL TGFβ1 decreased Epac1-expression in atrial fibroblasts, an effect blocked by pre-treatment with the Smad3-inhibitor SIS3 for 1 h before the addition of TGFβ1 for 48 h. (D) Norepinephrine (NE) significantly decreased Epac1-expression. Concomitant treatment with prazosin (PZ) and NE prevented NE-induced Epac1-reduction. (E) NE significantly increased collagen-I protein-expression. Immunoblots are shown (top), with corresponding mean data (bottom). (F) NE and concomitant treatment with PZ did not change COL1A1 mRNA-expression. (G) Phenylephrine (PE) decreased Epac1-expression. Each dot represents an individual independent experiment (*P < 0.05, **P < 0.01, ***P < 0.001; A, B, E, and G, unpaired t-test; C, D, and F, one-way ANOVA followed by Bonferroni correction).