Unravelling the Effects of Syndecan-4 Knockdown on Skeletal Muscle Functions

The remodelling of the extracellular matrix plays an important role in skeletal muscle development and regeneration. Syndecan-4 is a cell surface proteoglycan crucial for muscle differentiation. Syndecan-4−/− mice have been reported to be unable to regenerate following muscle damage. To investigate...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Sztretye Mónika
Singlár Zoltán
Ganbat Nyamkhuu
Al-Gaadi Dána
Szabó Kitti
Köhler Zoltán Márton
Dux László
Keller-Pintér Anikó
Csernoch László
Szentesi Péter
Dokumentumtípus: Cikk
Megjelent: 2023
Sorozat:INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES 24 No. 8
Tárgyszavak:
doi:10.3390/ijms24086933

mtmt:33742741
Online Access:http://publicatio.bibl.u-szeged.hu/28164
Leíró adatok
Tartalmi kivonat:The remodelling of the extracellular matrix plays an important role in skeletal muscle development and regeneration. Syndecan-4 is a cell surface proteoglycan crucial for muscle differentiation. Syndecan-4−/− mice have been reported to be unable to regenerate following muscle damage. To investigate the consequences of the decreased expression of Syndecan-4, we have studied the in vivo and in vitro muscle performance and the excitation–contraction coupling machinery in young and aged Syndecan-4+/− (SDC4) mice. In vivo grip force was decreased significantly as well as the average and maximal speed of voluntary running in SDC4 mice, regardless of their age. The maximal in vitro twitch force was reduced in both EDL and soleus muscles from young and aged SDC4 mice. Ca2+ release from the sarcoplasmic reticulum decreased significantly in the FDB fibres of young SDC4 mice, while its voltage dependence was unchanged regardless of age. These findings were present in muscles from young and aged mice as well. On C2C12 murine skeletal muscle cells, we have also found altered calcium homeostasis upon Syndecan-4 silencing. The decreased expression of Syndecan-4 leads to reduced skeletal muscle performance in mice and altered motility in C2C12 myoblasts via altered calcium homeostasis. The altered muscle force performance develops at an early age and is maintained throughout the life course of the animal until old age.
Terjedelem/Fizikai jellemzők:19
ISSN:1661-6596