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REGULATES MYOGENESIS AND MUSCLE REGENERATION
BY ACTIVATING p38 MAPK
1 Department of Medicine, Baylor College of Medicine, Houston, Texas, United States
* To whom correspondence should be addressed. E-mail: yiping{at}bcm.tmc.edu.
Although p38 MAPK activation is essential for myogenesis, the upstream signaling mechanism that activates p38 during myogenesis remains undefined. We recently reported that p38 activation, myogenesis, and regeneration in cardiotoxin-injured soleus muscle is impaired in TNF-
receptor double knockout (p55-/-p75-/-) mice. To fully evaluate the role of TNF- in myogenic activation of p38, we tried to determine if p38 activation in differentiating myoblasts requires autocrine TNF-, and whether forced activation of p38 rescues impaired myogenesis and regeneration in p55-/-p75-/- soleus. We observed an increase of TNF- release from C2C12 or mouse primary myoblasts placed in low serum differentiation medium. A TNF--neutralizing antibody added to differentiation medium blocked p38 activation, and suppressed differentiation markers MEF-2C, myogenin, p21 and myosin heavy chain in C2C12 myoblasts. Conversely, recombinant TNF- added to differentiation medium stimulated myogenesis at 0.05 ng/ml while inhibited it at 0.5 and 5 ng/ml. In addition, differentiation medium-induced p38 activation and myogenesis were compromised in primary myoblasts prepared from p55-/-p75-/- mice. Increased TNF- release was also seen in cardiotoxin-injured soleus over the course of regenetation. Forced activation of p38 via the constitutive activator of p38, MKK6bE, rescued impaired myogenesis and regeneration in cardiotoxin-injured p55-/-p75-/- soleus. These results indicate that TNF- regulates myogenesis and muscle regeneration as a key activator of p38.
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