| First Author | Hu SY | Year | 2012 |
| Journal | FEBS Lett | Volume | 586 |
| Issue | 19 | Pages | 3485-92 |
| PubMed ID | 22967900 | Mgi Jnum | J:190133 |
| Mgi Id | MGI:5448111 | Doi | 10.1016/j.febslet.2012.07.077 |
| Citation | Hu SY, et al. (2012) Progranulin compensates for blocked IGF-1 signaling to promote myotube hypertrophy in C2C12 myoblasts via the PI3K/Akt/mTOR pathway. FEBS Lett 586(19):3485-92 |
| abstractText | 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. |
