炎症
间充质干细胞
血小板
内吞作用
血小板活化
巨噬细胞
细胞生物学
癌症研究
医学
免疫学
病理
化学
生物
体外
受体
生物化学
内科学
作者
Qiyu Li,Zheyong Huang,Zhiqing Pang,Qiaozi Wang,Jinfeng Gao,Jing Chen,Zhengmin Wang,Haipeng Tan,Sam Li,Fei Xu,Jinxiang Chen,Muyin Liu,Xueyi Weng,Hongbo Yang,Yanan Song,Juying Qian,Junbo Ge
标识
DOI:10.1016/j.cej.2022.138992
摘要
Atherosclerosis is a major underlying cause of cardiovascular disease. Although certain success has been achieved in treatment for atherosclerosis, the risk of cardiovascular diseases still remains high. Anti-inflammation therapy was proved to halt atherosclerosis progression, but their clinical application was hindered by the systemic immunosuppressive effect. Since macrophages play a key role in the development of atherosclerosis, targeted delivery of anti-inflammatory therapeutics to lesional macrophages might be an effective therapeutic strategy to resolve localized inflammation while reducing the adverse effects. Mesenchymal stem cells derived extracellular vesicles (MSC-EVs) are believed to possess anti-atherosclerosis effects by reducing inflammation. In this study, we fabricated platelet mimetic MSC-EVs (P-EVs) by decorating EVs with platelets membranes. P-EVs inherited the natural homing ability of platelets to plaques and therapeutic effects of MSC-EVs. When injected into atherosclerotic mice, P-EVs were recruited to injured endothelium, then penetrated into plaques followed with endocytosis by inflammatory macrophages through the interaction between platelet membranes proteins and macrophages surface proteins. Subsequently, P-EVs delivered miRNAs into the cytoplasm of macrophages through lysosomal escape, which attenuated the progression of atherosclerosis eventually by switching the macrophage into anti-inflammatory phenotype, scavenging the overproduced ROS and reducing lipid deposition in lesional macrophages. In general, our study demonstrated the pro-resolving potential of P-EVs for targeted anti-inflammation therapy of atherosclerosis.
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