单位：[1]Department of Orthopaedic Surgery, Center for Osteonecrosis and Joint Preserving & Reconstruction, China-Japan Friendship Hospital, Beijing 100029, China[2]Department of Orthopaedic Surgery, Peking University China-Japan Friendship School of ClinicalMedicine, Beijing 100029, China
Osteonecrosis of the femoral head (ONFH) is a common clinical disease with a high disability rate. Injury of bone microvascular endothelial cells (BMECs) caused by glucocorticoid administration is one of the important causes of ONFH, and there is currently a lack of effective clinical treatments. Extracellular vesicles derived from bone stem cells (BMSC-EVs) can prevent ONFH by promoting angiogenesis and can inhibit cell apoptosis by regulating autophagy via the PI3K/Akt/mTOR signaling pathway. The present study aimed to investigate the effect of extracellular vesicles derived from bone marrow stem cells (BMSC) on a glucocorticoid-induced injury of BMECs and possible mechanisms. We found that BMSC-EVs attenuated glucocorticoid-induced viability, angiogenesis capacity injury, and the apoptosis of BMECs. BMSC-EVs increased the LC3 level, but decreased p62 (an autophagy protein receptor) expression, suggesting that BMSC-Exos activated autophagy in glucocorticoid-treated BMECs. The protective effects of BMSC-EVs on the glucocorticoid-induced injury of BMECs was mimicked by a known stimulator of autophagy (rapamycin) and could be enhanced by co-treatment with an autophagy inhibitor (LY294002). BMSC-EVs also suppressed the PI3K/Akt/mTOR signaling pathway, which regulates cell autophagy, in glucocorticoid-treated BMECs. In conclusion, the results indicate that BMSC-EVs prevent the glucocorticoid-induced injury of BMECs by regulating autophagy via the PI3K/Akt/mTOR pathway.
基金：
This project was supported by grants from the Beijing Natural Science Foundation
(7204301,7182146), Fundamental Research Funds for the Central Universities (3332021088), Elite Medical
Professionals project of China-Japan Friendship Hospital (NO.ZRJY2021-TD01, NO.ZRJY2021-
GG12), the National Natural Science Foundation of China (81672236, 81871830), the Ningxia Natural
Science Foundation (2020AAC03337), and the Joint Project of BRC-BC (Biomedical Translational
Engineering Research Center of BUCT-CJFH) (RZ2020-02).
第一作者单位：[1]Department of Orthopaedic Surgery, Center for Osteonecrosis and Joint Preserving & Reconstruction, China-Japan Friendship Hospital, Beijing 100029, China
共同第一作者：
通讯作者：
推荐引用方式(GB/T 7714)：
Ma Jinhui,Shen Mengran,Yue Debo,et al.Extracellular Vesicles from BMSCs Prevent Glucocorticoid-Induced BMECs Injury by Regulating Autophagy via the PI3K/Akt/mTOR Pathway[J].CELLS.2022,11(13):doi:10.3390/cells11132104.
APA：
Ma, Jinhui,Shen, Mengran,Yue, Debo,Wang, Weiguo,Gao, Fuqiang&Wang, Bailiang.(2022).Extracellular Vesicles from BMSCs Prevent Glucocorticoid-Induced BMECs Injury by Regulating Autophagy via the PI3K/Akt/mTOR Pathway.CELLS,11,(13)
MLA：
Ma, Jinhui,et al."Extracellular Vesicles from BMSCs Prevent Glucocorticoid-Induced BMECs Injury by Regulating Autophagy via the PI3K/Akt/mTOR Pathway".CELLS 11..13(2022)
