Progranulin compensates for blocked IGF-1 signaling to promote myotube hypertrophy in C2C12 myoblasts via the PI3K/Akt/mTOR pathway.

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.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Hu SY,Tai CC,Li YH,Wu JL

doi

10.1016/j.febslet.2012.07.077

subject

Has Abstract

pub_date

2012-09-21 00:00:00

pages

3485-92

issue

19

eissn

0014-5793

issn

1873-3468

pii

S0014-5793(12)00656-4

journal_volume

586

pub_type

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