miR-149 Alleviates Ox-LDL-Induced Endothelial Cell Injury by Promoting Autophagy through Akt/mTOR Pathway
Background. Atherosclerosis is a chronic process that takes place in the vascular wall and causes various cardiovascular diseases (CVDs). Micro-RNA-149 (miR-149) mediates many physiological and pathological processes, including atherosclerosis. However, it is unclear about the roles of miR-149 in en...
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| Format: | Article |
| Language: | English |
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Wiley
2021-01-01
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| Series: | Cardiology Research and Practice |
| Online Access: | http://dx.doi.org/10.1155/2021/9963258 |
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| author | Zhongsheng Zhu Jinyu Li Rui Tong Xiaorong Zhang Bo Yu |
| author_facet | Zhongsheng Zhu Jinyu Li Rui Tong Xiaorong Zhang Bo Yu |
| author_sort | Zhongsheng Zhu |
| collection | DOAJ |
| description | Background. Atherosclerosis is a chronic process that takes place in the vascular wall and causes various cardiovascular diseases (CVDs). Micro-RNA-149 (miR-149) mediates many physiological and pathological processes, including atherosclerosis. However, it is unclear about the roles of miR-149 in endothelial injury. Here, we explored the protective effect and related mechanism of miR-149 in endothelial cells induced with oxidized low-density lipoprotein (ox-LDL). Methods. Human endothelial cell lines (HUVECs) were exposed to ox-LDL to induce endothelial injury. Cell viability was determined by the CCK-8 assay. Autophagy was detected by immunofluorescence. RT-qPCR and western blot were carried out to determine the mRNA and protein expressions of Akt and mTOR. Results. The miR-149 level in HUVECs was reduced by ox-LDL (100 μg/mL) incubation in a time-dependent manner. miR-149-mimic transfection markedly protected HUVECs from ox-LDL-induced injury, with increased cell viability and reduced caspase-3 activity. miR-149 mimics enhanced HUVEC autophagy, which was induced initially by ox-LDL. miR-149 mimics also markedly downregulated the expression of Akt, p-Akt, mTOR, and p-mTOR in ox-LDL-treated HUVECs. The miR-149-induced protection against HUVECs injury could be reversed by cotreatment with 3-methyladenine (3-MA, an autophagy inhibitor) or insulin (an activator of Akt/mTOR pathway). Conclusions. miR-149 prevents ox-LDL-induced endothelial cell injury by enhancing autophagy via increasing Akt and mTOR expressions. |
| format | Article |
| id | doaj-art-e30c18e724654132afca67c4d6fa3b3c |
| institution | Kabale University |
| issn | 2090-8016 2090-0597 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Cardiology Research and Practice |
| spelling | doaj-art-e30c18e724654132afca67c4d6fa3b3c2025-02-03T05:44:47ZengWileyCardiology Research and Practice2090-80162090-05972021-01-01202110.1155/2021/99632589963258miR-149 Alleviates Ox-LDL-Induced Endothelial Cell Injury by Promoting Autophagy through Akt/mTOR PathwayZhongsheng Zhu0Jinyu Li1Rui Tong2Xiaorong Zhang3Bo Yu4Department of Cardiology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Pudong New District, Shanghai 201399, ChinaDepartment of Cardiology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Pudong New District, Shanghai 201399, ChinaDepartment of Cardiology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Pudong New District, Shanghai 201399, ChinaDepartment of Cardiology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Pudong New District, Shanghai 201399, ChinaDepartment of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Pudong New District, Shanghai 201399, ChinaBackground. Atherosclerosis is a chronic process that takes place in the vascular wall and causes various cardiovascular diseases (CVDs). Micro-RNA-149 (miR-149) mediates many physiological and pathological processes, including atherosclerosis. However, it is unclear about the roles of miR-149 in endothelial injury. Here, we explored the protective effect and related mechanism of miR-149 in endothelial cells induced with oxidized low-density lipoprotein (ox-LDL). Methods. Human endothelial cell lines (HUVECs) were exposed to ox-LDL to induce endothelial injury. Cell viability was determined by the CCK-8 assay. Autophagy was detected by immunofluorescence. RT-qPCR and western blot were carried out to determine the mRNA and protein expressions of Akt and mTOR. Results. The miR-149 level in HUVECs was reduced by ox-LDL (100 μg/mL) incubation in a time-dependent manner. miR-149-mimic transfection markedly protected HUVECs from ox-LDL-induced injury, with increased cell viability and reduced caspase-3 activity. miR-149 mimics enhanced HUVEC autophagy, which was induced initially by ox-LDL. miR-149 mimics also markedly downregulated the expression of Akt, p-Akt, mTOR, and p-mTOR in ox-LDL-treated HUVECs. The miR-149-induced protection against HUVECs injury could be reversed by cotreatment with 3-methyladenine (3-MA, an autophagy inhibitor) or insulin (an activator of Akt/mTOR pathway). Conclusions. miR-149 prevents ox-LDL-induced endothelial cell injury by enhancing autophagy via increasing Akt and mTOR expressions.http://dx.doi.org/10.1155/2021/9963258 |
| spellingShingle | Zhongsheng Zhu Jinyu Li Rui Tong Xiaorong Zhang Bo Yu miR-149 Alleviates Ox-LDL-Induced Endothelial Cell Injury by Promoting Autophagy through Akt/mTOR Pathway Cardiology Research and Practice |
| title | miR-149 Alleviates Ox-LDL-Induced Endothelial Cell Injury by Promoting Autophagy through Akt/mTOR Pathway |
| title_full | miR-149 Alleviates Ox-LDL-Induced Endothelial Cell Injury by Promoting Autophagy through Akt/mTOR Pathway |
| title_fullStr | miR-149 Alleviates Ox-LDL-Induced Endothelial Cell Injury by Promoting Autophagy through Akt/mTOR Pathway |
| title_full_unstemmed | miR-149 Alleviates Ox-LDL-Induced Endothelial Cell Injury by Promoting Autophagy through Akt/mTOR Pathway |
| title_short | miR-149 Alleviates Ox-LDL-Induced Endothelial Cell Injury by Promoting Autophagy through Akt/mTOR Pathway |
| title_sort | mir 149 alleviates ox ldl induced endothelial cell injury by promoting autophagy through akt mtor pathway |
| url | http://dx.doi.org/10.1155/2021/9963258 |
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