Syndecan-4 influences mammalian myoblast proliferation by modulating myostatin signalling and G1/S transition.
Myostatin, a TGF-beta superfamily member, is a negative regulator of muscle growth. Here we describe how myostatin activity is regulated by syndecan-4, a ubiquitous transmembrane heparan sulfate proteoglycan. During muscle regeneration the levels of both syndecan-4 and promyostatin decline gradually...
Elmentve itt :
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| Dokumentumtípus: | Cikk |
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2018
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| Sorozat: | FEBS LETTERS
592 No. 18 |
| doi: | 10.1002/1873-3468.13227 |
| mtmt: | 3418666 |
| Online Access: | http://publicatio.bibl.u-szeged.hu/14172 |
| Tartalmi kivonat: | Myostatin, a TGF-beta superfamily member, is a negative regulator of muscle growth. Here we describe how myostatin activity is regulated by syndecan-4, a ubiquitous transmembrane heparan sulfate proteoglycan. During muscle regeneration the levels of both syndecan-4 and promyostatin decline gradually after a sharp increase, concurrently with the release of mature myostatin. Promyostatin and syndecan-4 co-immunoprecipitate, and the interaction is heparinase-sensitive. ShRNA-mediated silencing of syndecan-4 reduces C2C12 myoblast proliferation via blocking the progression from G1- to S-phase of the cell cycle, which is accompanied by elevated levels of myostatin and p21(Waf1/Cip1), and decreases in cyclin E and cyclin D1 expression. Our results suggest that syndecan-4 functions as a reservoir for promyostatin regulating the local bioavailability of mature myostatin. This article is protected by copyright. All rights reserved. |
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| Terjedelem/Fizikai jellemzők: | 3139-3151 |
| ISSN: | 0014-5793 |