Department of Sports trauma & Arthroscopy, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, China.
Department of Sports trauma & Arthroscopy, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, China.
Acta Histochem. 2022 Oct;124(7):151933. doi: 10.1016/j.acthis.2022.151933. Epub 2022 Aug 4.
Greater bone resorption increases TGF-β1 release and nestin-positive BMSC recruitment to the subchondral bone marrow, leading to excessive subchondral osteophyte formation and severe wear to articular cartilage. Our previous research demonstrated that BMSCs-Exo attenuated cartilage damage in osteoarthritis (OA) rats through carrying highly expressed miR-135b.
The bone marrow mesenchymal stem cells (BMSCs) were isolated from mouse bone marrow, and BMSC-derived exosomes (BMSCs-Exo) were isolated from BMSCs. OA mouse models were established by anterior cruciate ligament transection (ACLT) surgery on the left knee of mice. Then we explored the therapeutic effect of BMSCs-Exo on ACLT mice.
BMSCs-Exo attenuated cartilage damage in OA mice in vivo by ameliorating articular cartilage degeneration and suppressing calcification of the cartilage zone. BMSCs-Exo also inhibited osteoclastogenesis by suppressing the MAPK pathway in vitro. Micro-computed tomography indicated that BMSCs-Exo impeded uncoupled subchondral bone remodeling. BMSCs-Exo also reduced CD31Emcn vessel activity in the subchondral bone and attenuated OA pain behaviors.
In conclusion, BMSCs-Exo maintains the microarchitecture, inhibits abnormal angiogenesis in subchondral bone and exerts protective effect against OA-induced pain and bone resorption on ACLT mice.
The datasets are available from the corresponding author on reasonable request.
破骨细胞吸收增加会导致 TGF-β1 释放和巢蛋白阳性骨髓间充质干细胞（BMSC）募集到软骨下骨骨髓，从而导致软骨下骨赘过度形成和关节软骨严重磨损。我们之前的研究表明，骨髓间充质干细胞来源的外泌体（BMSCs-Exo）通过携带高表达的 miR-135b 来减轻骨关节炎（OA）大鼠的软骨损伤。
从鼠骨髓中分离骨髓间充质干细胞（BMSCs），并从 BMSCs 中分离 BMSC 衍生的外泌体（BMSCs-Exo）。通过对小鼠左膝关节前交叉韧带切断（ACLT）手术建立 OA 小鼠模型。然后，我们探索了 BMSCs-Exo 对 ACLT 小鼠的治疗效果。
BMSCs-Exo 通过改善关节软骨退变和抑制软骨区钙化，在体内减轻 OA 小鼠的软骨损伤。BMSCs-Exo 还通过抑制 MAPK 通路在体外抑制破骨细胞生成。微计算机断层扫描表明，BMSCs-Exo 阻碍了软骨下骨的脱耦联重塑。BMSCs-Exo 还降低了软骨下骨中 CD31Emcn 血管的活性，并减轻了 OA 引起的疼痛行为。
总之，BMSCs-Exo 维持微结构，抑制软骨下骨异常血管生成，并对 ACLT 小鼠的 OA 诱导性疼痛和骨吸收发挥保护作用。
数据集可应合理要求向相应作者索取。
