| First Author | Li Y | Year | 2023 |
| Journal | Bone Res | Volume | 11 |
| Issue | 1 | Pages | 24 |
| PubMed ID | 37156778 | Mgi Jnum | J:355524 |
| Mgi Id | MGI:7715003 | Doi | 10.1038/s41413-023-00252-1 |
| Citation | Li Y, et al. (2023) Neutralization of excessive levels of active TGF-beta1 reduces MSC recruitment and differentiation to mitigate peritendinous adhesion. Bone Res 11(1):24 |
| abstractText | Peritendinous adhesion formation (PAF) can substantially limit the range of motion of digits. However, the origin of myofibroblasts in PAF tissues is still unclear. In this study, we found that the concentration of active TGF-beta1 and the numbers of macrophages, mesenchymal stromal cells (MSCs), and myofibroblasts in human and mouse adhesion tissues were increased. Furthermore, knockout of TGF-beta1 in macrophages or TGF-beta1R2 in MSCs inhibited PAF by reducing MSC and myofibroblast infiltration and collagen I and III deposition, respectively. Moreover, we found that MSCs differentiated into myofibroblasts to form adhesion tissues. Systemic injection of the TGF-beta-neutralizing antibody 1D11 during the granulation formation stage of PAF significantly reduced the infiltration of MSCs and myofibroblasts and, subsequently, PAF. These results suggest that macrophage-derived TGF-beta1 recruits MSCs to form myofibroblasts in peritendinous adhesions. An improved understanding of PAF mechanisms could help identify a potential therapeutic strategy. |
