间充质干细胞
炎症
癌症研究
细胞生物学
骨关节炎
电穿孔
骨髓
巨噬细胞极化
破骨细胞
体内
软骨
细胞外基质
化学
医学
祖细胞
干细胞
SIRT2
骨重建
巨噬细胞
生物发光成像
骨愈合
趋化性
胞外囊泡
体外
关节炎
组织工程
免疫学
细胞疗法
转染
促炎细胞因子
纳米笼
移植
表型
作者
Jie Zhou,Zhiling Zhang,Shuang Fu,Lulu Xu,Yukang Wang,Zhihui Hu,Adam C. Midgley,Yufei Liu,Shufang Wang
出处
期刊:Small
[Wiley]
日期:2025-09-29
卷期号:21 (46): e04482-e04482
被引量:1
标识
DOI:10.1002/smll.202504482
摘要
Temporomandibular joint osteoarthritis (TMJ-OA), a refractory osteoarticular disorder, is critically hindered by inflammation-mediated bone metabolic imbalance during disease progression. Building on the previous discovery that inflammation-indued mesenchymal stem cell-derived small extracellular vesicles (sEV) regulate macrophage polarization via the miR-27b-3p/CSF-1 axis, functionally enhanced engineered sEV (sEV-r) is developed through 3D dynamic culture coupled with electroporation technology. This strategy leverages 3D culture to optimize vesicle bioactivity and employs electroporation for high-efficiency miR-27b-3p loading, endowing sEV-r with both inherent targeting capacity and amplified anti-inflammatory functionality. Experimental validation demonstrate that sEV-r effectively suppresses CSF-1-driven inflammatory cascades via efficient miR-27b-3p delivery while enhancing the chemotactic migration of bone marrow mesenchymal stem cells (BMSCs). In vivo studies demonstrate that sEV-r exhibits superior therapeutic efficacy in both acute inflammatory (mouse ear edema) and chronic osteoarthritic (TMJ-OA) models. In TMJ-OA models, sEV-r exert dual therapeutic mechanisms: modulating macrophage phenotype polarization to optimize the inflammatory microenvironment, and inhibiting oxidative stress to block abnormal osteoclast activation. These effects collectively improve subchondral bone microstructure and restore bone metabolic equilibrium. This study establishes a novel engineering strategy for sEV-based targeted therapy, providing critical insights into precision interventions for TMJ-OA.
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