Bibliographic Details
| Title: |
Extracellular Vesicles from BMSCs Prevent Glucocorticoid-Induced BMECs Injury by Regulating Autophagy via the PI3K/Akt/mTOR Pathway |
| Authors: |
Jinhui Ma, Mengran Shen, Debo Yue, Weiguo Wang, Fuqiang Gao, Bailiang Wang |
| Source: |
Cells, Vol 11, Iss 13, p 2104 (2022) |
| Publisher Information: |
MDPI AG, 2022. |
| Publication Year: |
2022 |
| Collection: |
LCC:Cytology |
| Subject Terms: |
autophagy, extracellular vesicles, PI3K/Akt/mTOR pathway, bone marrow mesenchymal stem cells, bone microvascular endothelial cells, Cytology, QH573-671 |
| More Details: |
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. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
2073-4409 |
| Relation: |
https://www.mdpi.com/2073-4409/11/13/2104; https://doaj.org/toc/2073-4409 |
| DOI: |
10.3390/cells11132104 |
| Access URL: |
https://doaj.org/article/1ef9acba9fab477384c5e1ba5e21892c |
| Accession Number: |
edsdoj.1ef9acba9fab477384c5e1ba5e21892c |
| Database: |
Directory of Open Access Journals |
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