Improvement of Myocardial Cell Injury by miR-199a-3p/mTOR Axis through Regulating Cell Apoptosis and Autophagy
Background. Myocardial ischemia-reperfusion injury (MIRI) is characterized by its high incidence rate and mortality. miR-199a-3p is thought to be strongly linked with the development of some myocardial diseases, but the influence of miR-199a-3p in MIRI remains unclear. Methods. AC16 cells were used....
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2022-01-01
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| Series: | Journal of Immunology Research |
| Online Access: | http://dx.doi.org/10.1155/2022/1642301 |
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| author | Weixiong Wu Xingfeng Chen Qingyang Hu Xuefei Wang Jingyu Zhu Qianzhen Li |
| author_facet | Weixiong Wu Xingfeng Chen Qingyang Hu Xuefei Wang Jingyu Zhu Qianzhen Li |
| author_sort | Weixiong Wu |
| collection | DOAJ |
| description | Background. Myocardial ischemia-reperfusion injury (MIRI) is characterized by its high incidence rate and mortality. miR-199a-3p is thought to be strongly linked with the development of some myocardial diseases, but the influence of miR-199a-3p in MIRI remains unclear. Methods. AC16 cells were used. The concentrations of mammalian target of rapamycin (mTOR), light chain 3 II/light chain 3 I, and Beclin-1 were detected with western blotting and qRT-PCR. The binding site between mTOR and miR-199a-3p was evaluated via luciferase report assay. Cell apoptosis was evaluated through flow cytometry. Results. Knockdown of miR-199a-3p accelerated the myocardial cell injury after L-oxygen treatment. Increased expression of mTOR and suppressed autophagy were observed after knockdown of miR-199a-3p. Knockdown of miR-199a-3p or overexpression of mTOR greatly aggravated cell injury through inhibiting autophagy. Conclusions. This study might be helpful for the therapeutic method of MIRI through by regulating miR-199a-3p/mTOR. |
| format | Article |
| id | doaj-art-d76232b6f558495781582f02a1b7bbd9 |
| institution | OA Journals |
| issn | 2314-7156 |
| language | English |
| publishDate | 2022-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Immunology Research |
| spelling | doaj-art-d76232b6f558495781582f02a1b7bbd92025-08-20T02:20:09ZengWileyJournal of Immunology Research2314-71562022-01-01202210.1155/2022/1642301Improvement of Myocardial Cell Injury by miR-199a-3p/mTOR Axis through Regulating Cell Apoptosis and AutophagyWeixiong Wu0Xingfeng Chen1Qingyang Hu2Xuefei Wang3Jingyu Zhu4Qianzhen Li5Department of Cardiovascular SurgeryDepartment of Cardiovascular SurgeryDepartment of Cardiovascular SurgeryDepartment of Cardiovascular SurgeryDepartment of Cardiovascular SurgeryDepartment of Cardiovascular SurgeryBackground. Myocardial ischemia-reperfusion injury (MIRI) is characterized by its high incidence rate and mortality. miR-199a-3p is thought to be strongly linked with the development of some myocardial diseases, but the influence of miR-199a-3p in MIRI remains unclear. Methods. AC16 cells were used. The concentrations of mammalian target of rapamycin (mTOR), light chain 3 II/light chain 3 I, and Beclin-1 were detected with western blotting and qRT-PCR. The binding site between mTOR and miR-199a-3p was evaluated via luciferase report assay. Cell apoptosis was evaluated through flow cytometry. Results. Knockdown of miR-199a-3p accelerated the myocardial cell injury after L-oxygen treatment. Increased expression of mTOR and suppressed autophagy were observed after knockdown of miR-199a-3p. Knockdown of miR-199a-3p or overexpression of mTOR greatly aggravated cell injury through inhibiting autophagy. Conclusions. This study might be helpful for the therapeutic method of MIRI through by regulating miR-199a-3p/mTOR.http://dx.doi.org/10.1155/2022/1642301 |
| spellingShingle | Weixiong Wu Xingfeng Chen Qingyang Hu Xuefei Wang Jingyu Zhu Qianzhen Li Improvement of Myocardial Cell Injury by miR-199a-3p/mTOR Axis through Regulating Cell Apoptosis and Autophagy Journal of Immunology Research |
| title | Improvement of Myocardial Cell Injury by miR-199a-3p/mTOR Axis through Regulating Cell Apoptosis and Autophagy |
| title_full | Improvement of Myocardial Cell Injury by miR-199a-3p/mTOR Axis through Regulating Cell Apoptosis and Autophagy |
| title_fullStr | Improvement of Myocardial Cell Injury by miR-199a-3p/mTOR Axis through Regulating Cell Apoptosis and Autophagy |
| title_full_unstemmed | Improvement of Myocardial Cell Injury by miR-199a-3p/mTOR Axis through Regulating Cell Apoptosis and Autophagy |
| title_short | Improvement of Myocardial Cell Injury by miR-199a-3p/mTOR Axis through Regulating Cell Apoptosis and Autophagy |
| title_sort | improvement of myocardial cell injury by mir 199a 3p mtor axis through regulating cell apoptosis and autophagy |
| url | http://dx.doi.org/10.1155/2022/1642301 |
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