| First Author | Wasnik S | Year | 2019 |
| Journal | Sci Adv | Volume | 5 |
| Issue | 7 | Pages | eaaw2108 |
| PubMed ID | 31392271 | Mgi Jnum | J:290847 |
| Mgi Id | MGI:6435435 | Doi | 10.1126/sciadv.aaw2108 |
| Citation | Wasnik S, et al. (2019) Cyclooxygenase 2 augments osteoblastic but suppresses chondrocytic differentiation of CD90(+) skeletal stem cells in fracture sites. Sci Adv 5(7):eaaw2108 |
| abstractText | Cyclooxygenase 2 (COX-2) is essential for normal tissue repair. Although COX-2 is known to enhance the differentiation of mesenchymal stem cells (MSCs), how COX-2 regulates MSC differentiation into different tissue-specific progenitors to promote tissue repair remains unknown. Because it has been shown that COX-2 is critical for normal bone repair and local COX-2 overexpression in fracture sites accelerates fracture repair, this study aimed to determine the MSC subsets that are targeted by COX-2. We showed that CD90(+) mouse skeletal stem cells (mSSCs; i.e., CD45(-)Tie2(-)AlphaV(+) MSCs) were selectively recruited by macrophage/monocyte chemoattractant protein 1 into fracture sites following local COX-2 overexpression. In addition, local COX-2 overexpression augmented osteoblast differentiation and suppressed chondrocyte differentiation in CD90(+) mSSCs, which depended on canonical WNT signaling. CD90 depletion data demonstrated that local COX-2 overexpression targeted CD90(+) mSSCs to accelerate fracture repair. In conclusion, CD90(+) mSSCs are promising targets for the acceleration of bone repair. |
