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. 2019 Apr 24;10(4):903–918. doi: 10.1002/jcsm.12434

Figure 2.

Figure 2

Ex‐4 regulates the expression of MSTN through GLP‐1R‐mediated PKA and AKT signalling pathways. (A) The protein expression level of GLP‐1R in the pancreas and TA muscle from WT (Glp1r +/+ Cre −), heterozygous (Glp1r flox/+ Cre +), and homozygous (Glp1r flox/flox Cre +) mice with a representative blot. (B) C2C12 myotubes were pretreated with 20 nM of Ex‐9 (GLP‐1R antagonist) for 10 min and then were further treated with 20 nM of Ex‐4 for 30 min. cAMP production was measured using cAMP ELISA kit. (C–E) The treated C2C12 myotubes were examined for the activation of GLP‐1R downstream mediators including PKA and HSF‐1 (C) and AKT and NF‐κB (D) signals using western blot. (E) The protein level of MSTN with a representative blot. (F–I) GLP‐1R siRNA‐transfected C2C12 myotubes were treated with 20 nM Ex‐4 for 30 min. (F) Representative blot of GLP‐1R protein levels. (G–I) C2C12 myotubes were examined for the activation of downstream mediators of GLP‐1R, including PKA and HSF‐1 (G) and AKT and NF‐κB (H) by western blotting. (I) Representative blot of MSTN protein levels. All values are expressed as the mean ± standard error. Significant differences are indicated as **P < 0.01 compared with Con + vehicle. n = 3. Con, control; Ex‐4, exendin‐4; Ex‐9, exendin‐9.