[HTML][HTML] Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration
A Pisconti, GB Banks, F Babaeijandaghi, ND Betta… - Skeletal muscle, 2016 - Springer
Skeletal muscle, 2016•Springer
Background The skeletal muscle stem cell niche provides an environment that maintains
quiescent satellite cells, required for skeletal muscle homeostasis and regeneration.
Syndecan-3, a transmembrane proteoglycan expressed in satellite cells, supports
communication with the niche, providing cell interactions and signals to maintain quiescent
satellite cells. Results Syndecan-3 ablation unexpectedly improves regeneration in
repeatedly injured muscle and in dystrophic mice, accompanied by the persistence of …
quiescent satellite cells, required for skeletal muscle homeostasis and regeneration.
Syndecan-3, a transmembrane proteoglycan expressed in satellite cells, supports
communication with the niche, providing cell interactions and signals to maintain quiescent
satellite cells. Results Syndecan-3 ablation unexpectedly improves regeneration in
repeatedly injured muscle and in dystrophic mice, accompanied by the persistence of …
Background
The skeletal muscle stem cell niche provides an environment that maintains quiescent satellite cells, required for skeletal muscle homeostasis and regeneration. Syndecan-3, a transmembrane proteoglycan expressed in satellite cells, supports communication with the niche, providing cell interactions and signals to maintain quiescent satellite cells.
Results
Syndecan-3 ablation unexpectedly improves regeneration in repeatedly injured muscle and in dystrophic mice, accompanied by the persistence of sublaminar and interstitial, proliferating myoblasts. Additionally, muscle aging is improved in syndecan-3 null mice. Since syndecan-3 null myofiber-associated satellite cells downregulate Pax7 and migrate away from the niche more readily than wild type cells, syxndecan-3 appears to regulate satellite cell homeostasis and satellite cell homing to the niche.
Conclusions
Manipulating syndecan-3 provides a promising target for development of therapies to enhance muscle regeneration in muscular dystrophies and in aged muscle.
Springer