Progranulin compensates for blocked IGF-1 signaling to promote myotube hypertrophy in C2C12 myoblasts via the PI3K/Akt/mTOR pathway |
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Authors: | Shao-Yang Hu Chen-Chen Tai Yen-Hsing LiJen-Leih Wu |
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Affiliation: | a Department of Biological Science and Technology, National Pingtung University of Science and Technology, Pingtung 912, Taiwan b Institute of Cellular and Organismic Biology, Academia Sinica, Taipei 115, Taiwan |
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Abstract: | 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. |
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Keywords: | Progranulin IGF-1 Muscle hypertrophy C2C12 myoblast Signaling |
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