Department of Orthopaedic Surgery, Washington University School of Medicine, St. Louis, MO, USA.
Stem Cells. 2023 Jun 15;41(6):617-627. doi: 10.1093/stmcls/sxad032.
Achilles tendon rupture is a common sports-related injury. Even with advanced clinical treatments, many patients suffer from long-term pain and functional deficits. These unsatisfactory outcomes result primarily from an imbalanced injury response with excessive inflammation and inadequate tendon regeneration. Prior studies showed that extracellular vesicles from inflammation-primed adipose-derived stem cells (iEVs) can attenuate early tendon inflammatory response to injury. It remains to be determined if iEVs can both reduce inflammation and promote regeneration in the later phases of tendon healing and the underlying mechanism. Therefore, this study investigated the mechanistic roles of iEVs in regulating tendon injury response using a mouse Achilles tendon injury and repair model in vivo and iEV-macrophage and iEV-tendon cell coculture models in vitro. Results showed that iEVs promoted tendon anti-inflammatory gene expression and reduced mononuclear cell accumulation to the injury site in the remodeling phase of healing. iEVs also increased collagen deposition in the injury center and promoted tendon structural recovery. Accordingly, mice treated with iEVs showed less peritendinous scar formation, much lower incidence of postoperative tendon gap or rupture, and faster functional recovery compared to untreated mice. Further in vitro studies revealed that iEVs both inhibited macrophage M1 polarization and increased tendon cell proliferation and collagen production. The iEV effects were partially mediated by miR-147-3p, which blocked the toll-like receptor 4/NF-κB signaling pathway that activated the M1 phenotype of macrophages. The combined results demonstrate that iEVs are a promising therapeutic agent that can enhance tendon repair by attenuating inflammation and promoting intrinsic healing.
跟腱断裂是一种常见的与运动相关的损伤。即使采用先进的临床治疗方法,许多患者仍长期遭受疼痛和功能障碍。这些不理想的结果主要是由于损伤反应失衡,表现为过度炎症和不充分的跟腱再生。先前的研究表明,来自炎症预刺激脂肪来源干细胞的细胞外囊泡(iEVs)可以减轻损伤后早期跟腱的炎症反应。然而,iEVs 是否可以在跟腱愈合的后期阶段既减轻炎症又促进再生,以及潜在的机制仍有待确定。因此,本研究使用体内小鼠跟腱损伤和修复模型以及体外 iEV-巨噬细胞和 iEV-肌腱细胞共培养模型,研究了 iEV 调节跟腱损伤反应的机制作用。结果表明,iEVs 促进了肌腱抗炎基因的表达,并减少了单核细胞在愈合重塑阶段向损伤部位的聚集。iEVs 还增加了损伤中心的胶原蛋白沉积,并促进了肌腱结构的恢复。因此,与未治疗的小鼠相比,接受 iEV 治疗的小鼠表现出更少的腱周瘢痕形成、更低的术后肌腱间隙或断裂发生率以及更快的功能恢复。进一步的体外研究表明,iEVs 既抑制了巨噬细胞 M1 极化,又增加了肌腱细胞的增殖和胶原蛋白的产生。iEV 的作用部分是由 miR-147-3p 介导的,它阻断了激活巨噬细胞 M1 表型的 toll 样受体 4/NF-κB 信号通路。综合结果表明,iEVs 是一种很有前途的治疗剂,通过减轻炎症和促进内在愈合来增强肌腱修复。