Fig. 3
From: JNK regulates muscle remodeling via myostatin/SMAD inhibition
SMAD-linker and JNK phosphorylation with exercise and muscle contraction in mice. a ICR mice underwent moderate intensity treadmill running for 15, 30, or 60 min and gastrocnemius muscles were collected. Control (rest) mice did not undergo treadmill running. Western blotting was used to determine exercise-induced signal transduction. Data from N = 3 mice/group are shown. b Electrodes were used to stimulate the lower hindlimb muscles from ICR mice [C; contracted]. The contralateral limb was unstimulated and acted as a control [B; basal]. Data from N = 3 mice/group are shown. c Both soleus muscles were rapidly removed from mice and attached to a force tranducer in oxygenated Kreb’s Henseleit Buffer. One muscle from each mouse was left at resting tension and acted as a basal control [Basal; B], while contralateral muscle was stretched for 10 min at a force of 0.12 N [Stretched; S]. N = 6 independent experiments were performed, and individual results from N = 3 are shown. pSMAD2L, linker region phosphorylated SMAD2; pJNK, phosphorylated (active) C-Jun N-terminal Kinase; pAMPK, phosphorylated (T172) AMP-activated protein kinase; pERK, phosphorylated extracellular signal regulated kinase; pP38, phosphorylated P38 Mitogen-Activated Protein Kinase; SMAD2, Total SMAD2. Images obtained using stain-free gel technology (Bio-Rad) that allows for total protein visualization and quantification are shown as a loading control (Loading)
