| First Author | Xiao H | Year | 2022 |
| Journal | Elife | Volume | 11 |
| PubMed ID | 35475783 | Mgi Jnum | J:324461 |
| Mgi Id | MGI:7278269 | Doi | 10.7554/eLife.73614 |
| Citation | Xiao H, et al. (2022) Mechanical stimulation promotes enthesis injury repair by mobilizing Prrx1(+) cells via ciliary TGF-beta signaling. Elife 11:e73614 |
| abstractText | Proper mechanical stimulation can improve rotator cuff enthesis injury repair. However, the underlying mechanism of mechanical stimulation promoting injury repair is still unknown. In this study, we found that Prrx1(+) cell was essential for murine rotator cuff enthesis development identified by single-cell RNA sequence and involved in the injury repair. Proper mechanical stimulation could promote the migration of Prrx1(+) cells to enhance enthesis injury repair. Meantime, TGF-beta signaling and primary cilia played an essential role in mediating mechanical stimulation signaling transmission. Proper mechanical stimulation enhanced the release of active TGF-beta1 to promote migration of Prrx1(+) cells. Inhibition of TGF-beta signaling eliminated the stimulatory effect of mechanical stimulation on Prrx1(+) cell migration and enthesis injury repair. In addition, knockdown of Pallidin to inhibit TGF-betaR2 translocation to the primary cilia or deletion of Ift88 in Prrx1(+) cells also restrained the mechanics-induced Prrx1(+) cells migration. These findings suggested that mechanical stimulation could increase the release of active TGF-beta1 and enhance the mobilization of Prrx1(+) cells to promote enthesis injury repair via ciliary TGF-beta signaling. |
