细胞生物学
血管生成
骨愈合
化学
微泡
焦点粘着
间充质干细胞
再生(生物学)
细胞外基质
生物
癌症研究
解剖
信号转导
生物化学
小RNA
基因
作者
Pengzhen Cheng,Tianqing Cao,Xueyi Zhao,Weiguang Lu,Sheng Miao,Fenru Ning,Dong Wang,Yi Gao,Long Wang,Guoxian Pei,Liu Yang
标识
DOI:10.1016/j.bioactmat.2021.10.021
摘要
The technique bottleneck of repairing large bone defects with tissue engineered bone is the vascularization of tissue engineered grafts. Although some studies have shown that extracellular vesicles (EVs) derived from bone marrow mesenchymal stem cells (BMSCs) promote bone healing and repair by accelerating angiogenesis, the effector molecules and the mechanism remain unclear, which fail to provide ideas for the future research and development of cell-free interventions. Here, we found that Nidogen1-enriched EV (EV-NID1) derived from BMSCs interferes with the formation and assembly of focal adhesions (FAs) by targeting myosin-10, thereby reducing the adhesion strength of rat arterial endothelial cells (RAECs) to the extracellular matrix (ECM), and enhancing the migration and angiogenesis potential of RAECs. Moreover, by delivery with composite hydrogel, EV-NID1 is demonstrated to promote angiogenesis and bone regeneration in rat femoral defects. This study identifies the intracellular binding target of EV-NID1 and further elucidates a novel approach and mechanism, thereby providing a cell-free construction strategy with precise targets for the development of vascularized tissue engineering products.
科研通智能强力驱动
Strongly Powered by AbleSci AI