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. 2016 May 20;4(10):e12791. doi: 10.14814/phy2.12791

Figure 6.

Figure 6

Expression of β 2‐AR, Epac1/2, PDE4D and PKA in TA and SOL muscles prepared from WT and Epac1KO at baseline. (A) Representative immunoblotting results of total β 2‐AR, Epac1/2, PDE4D‐L (long isoforms), PDE4D‐S (short isoforms), and PKA in TA and SOL prepared from WT or Epac1KO at baseline. (B) Expression of β 2‐AR, Epac1/2, PDE4D‐L, PDE4D‐S, and PKA in TA muscle and SOL muscle prepared from WT at baseline. The expression of each molecule in SOL was significantly greater than that in TA (**P < 0.01, ***P < 0.001 vs. TA by unpaired t‐test, n = 4–5), but the magnitude of the increase of PDE4D‐L was much greater (12‐fold), compared to β 2‐AR (7.6‐fold), Epac1 (5.1‐fold), Epac2 (2.8‐fold) and PDE4D‐S (1.7‐fold) and PKA (3.3‐fold). The amount of expression in TA muscle of WT treated with saline (Control in WT) was taken as 100% in each determination. (C) Expression of β 2‐AR, Epac1/2, PDE4D‐L, PDE4D‐S, and PKA in TA and SOL prepared from Epac1KO at baseline. The expression of each molecule in SOL was similarly and significantly greater than that in TA (**P < 0.01 vs. TA by unpaired t‐test, n = 4–5), but the magnitude of the increase of PDE4D‐L (11‐fold) was much greater, compared to those of β 2‐AR (2.8‐fold), Epac2 (10.1‐fold), PDE4D‐S (1.8‐fold), and PKA (4.2‐fold). The amount of expression in TA muscle of Epac1KO treated with saline (Control in Epac1KO) was taken as 100% in each determination.