| First Author | Pisconti A | Year | 2016 |
| Journal | Skelet Muscle | Volume | 6 |
| Pages | 34 | PubMed ID | 27757223 |
| Mgi Jnum | J:328168 | Mgi Id | MGI:6838538 |
| Doi | 10.1186/s13395-016-0104-8 | Citation | Pisconti A, et al. (2016) Loss of niche-satellite cell interactions in syndecan-3 null mice alters muscle progenitor cell homeostasis improving muscle regeneration. Skelet Muscle 6:34 |
| abstractText | 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. |
