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Progranulin compensates for blocked IGF‐1 signaling to promote myotube hypertrophy in C2C12 myoblasts via the PI3K/Akt/mTOR pathway
Author(s) -
Hu Shao-Yang,
Tai Chen-Chen,
Li Yen-Hsing,
Wu Jen-Leih
Publication year - 2012
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2012.07.077
Subject(s) - c2c12 , pi3k/akt/mtor pathway , protein kinase b , signal transduction , muscle hypertrophy , growth factor , endocrinology , myocyte , medicine , biology , muscle atrophy , microbiology and biotechnology , skeletal muscle , phenotype , receptor , myogenesis , genetics , gene
It is well known that growth hormone (GH)‐induced IGF‐1 signaling plays a dominant role in postnatal muscle growth. Our previous studies have identified a growth factor, progranulin (PGRN), that is co‐induced with IGF‐1 upon GH administration. This result prompted us to explore the function of PGRN and its association with IGF‐1. In the present study, we demonstrated that, similar to IGF‐1, PGRN can promote C2C12 myotube hypertrophy via the PI(3)K/Akt/mTOR pathway. Moreover, PGRN can rescue the muscle atrophy phenotypes in C2C12 myotube when IGF‐1 signaling is blocked. This result shows that PGRN can substitute for IGF‐1 signaling in the regulation of muscle growth. Our findings provide new insights into IGF‐1‐modulated complicated networks that regulate muscle growth.