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. 2012 May;166(2):676–688. doi: 10.1111/j.1476-5381.2011.01785.x

Figure 5.

Figure 5

Inhibition of Epac/PKCδ pathway prevented β-adrenoceptor-induced p38 MAPK activation. (A) After knock-down of Epac1 by adenovirus, cells were stimulated with isoprenaline (10 µM; ISO) for 5 min and p38 MAPK phosphorylation was measured by immunoblot analysis. **P < 0.01 vs. control, ##P < 0.01 PKCδ-shRNAs vs. scrambled, n= 3. (B) NMCFs were pretreated with PKCδ translocation inhibitor (δV1-1, 5 µM), or control peptide for 30 min and incubated with isoprenaline (10 µM) for 5 min. p38 MAPK phosphorylation was measured by immunoblot analysis. **P < 0.01 vs. Con. NS, isoprenaline vs. Con in δV1-1 group, n= 3. (C) After knock-down of PKCδ by adenovirus, cells were stimulated with isoprenaline (10 µM) for 5 min and p38 MAPK phosphorylation was measured by immunoblot analysis. **P < 0.01 vs. control, ##P < 0.01 PKCδ-shRNAs vs. scrambled, n= 3.