Deletion of cytosolic phospholipase A2 promotes striated muscle growth.

摘要: Generation of arachidonic acid by the ubiquitously expressed cytosolic phospholipase A2 (PLA2) has a fundamental role in regulation cellular homeostasis, inflammation and tumorigenesis. Here we report that PLA2 is negative regulator growth, specifically striated muscle. We find normal growth skeletal muscle, as well pathologic stress-induced hypertrophic heart, are exaggerated Pla2g4a-/- mice, which lack gene encoding PLA2. The mechanism underlying this phenotype negatively regulates insulin-like factor (IGF)-1 signaling. Absence leads to sustained activation IGF-1 pathway, results from failure 3-phosphoinositide-dependent protein kinase (PDK)-1 recruit phosphorylate C (PKC)-zeta, Arachidonic restores PKC-zeta, correcting These indicate regulate muscle modulating multiple growth-regulatory pathways.