Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis
Background. Myocardial infarction (MI) is cardiac tissue necrosis caused by acute and persistent ischemic hypoxia of the coronary arteries. This study is aimed at investigating the expression of long noncoding RNA (lncRNA) LINC00261 in MI and its effect on myocardial cells. Methods. qRT-PCR was perf...
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| Format: | Article |
| Language: | English |
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Wiley
2021-01-01
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| Series: | Cardiovascular Therapeutics |
| Online Access: | http://dx.doi.org/10.1155/2021/6628194 |
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| _version_ | 1832549154683879424 |
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| author | Chaoxin Jiang Qing Zhao Chenlong Wang Minyan Peng Guoqing Hao Zhifeng Liu Wenjin Fu Kewei Zhao |
| author_facet | Chaoxin Jiang Qing Zhao Chenlong Wang Minyan Peng Guoqing Hao Zhifeng Liu Wenjin Fu Kewei Zhao |
| author_sort | Chaoxin Jiang |
| collection | DOAJ |
| description | Background. Myocardial infarction (MI) is cardiac tissue necrosis caused by acute and persistent ischemic hypoxia of the coronary arteries. This study is aimed at investigating the expression of long noncoding RNA (lncRNA) LINC00261 in MI and its effect on myocardial cells. Methods. qRT-PCR was performed to detect the expression levels of LINC00261, miR-522-3p, and TNRC6A in normal and MI cells. Western blotting analysis was performed to detect the expression of TNRC6A protein. Viability and apoptosis of myocardial cells after MI with the knockout of LINC00261 or TNRC6A were detected. The relationships among miR-522-3p, LINC00261, and TNRC6A in cardiomyocytes were evaluated using a double luciferase reporter gene assay. Hypoxic preconditioning in normal cells was used to construct a simulated MI environment to investigate the effect of LINC00261 on apoptosis of cardiac cells. Results. LINC00261 and TNRC6A were upregulated, while miR-522-3p was downregulated in coronary heart disease tissues with MI. Knockout of LINC00261 can increase the viability of cardiomyocytes and inhibit cell apoptosis. LINC00261 targets miR-522-3p in cardiomyocytes. In addition, miR-522-3p targets TNRC6A in cardiomyocytes. TNRC6A regulates cell viability and apoptosis of cardiomyocytes after MI, and TNRC6A-induced MI can be reversed by overexpression of miR-522-3p. Conclusions. LINC00261 downregulated miR-522-3p in cardiomyocytes after MI by directly targeting miR-522-3p. TNRC6A is the direct target of miR-522-3p. Our results indicated that LINC00261 might serve as a therapeutic target for the treatment of MI. |
| format | Article |
| id | doaj-art-3a65fa9f34dc4fb586289852d8aceebe |
| institution | Kabale University |
| issn | 1755-5914 1755-5922 |
| language | English |
| publishDate | 2021-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Cardiovascular Therapeutics |
| spelling | doaj-art-3a65fa9f34dc4fb586289852d8aceebe2025-02-03T06:12:04ZengWileyCardiovascular Therapeutics1755-59141755-59222021-01-01202110.1155/2021/66281946628194Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) AxisChaoxin Jiang0Qing Zhao1Chenlong Wang2Minyan Peng3Guoqing Hao4Zhifeng Liu5Wenjin Fu6Kewei Zhao7Department of Clinical Laboratory, Guangdong Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Foshan, Guangdong 528200, ChinaDepartment of Clinical Laboratory, The Third Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510240, ChinaDepartment of Laboratory Medicine, Nanhai Hospital, Southern Medical University, Foshan, Guangdong 528244, ChinaDepartment of Clinical Laboratory, Guangdong Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Foshan, Guangdong 528200, ChinaDepartment of Clinical Laboratory, Guangdong Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Foshan, Guangdong 528200, ChinaDepartment of Clinical Laboratory, Guangdong Provincial Hospital of Integrated Traditional Chinese and Western Medicine, Foshan, Guangdong 528200, ChinaDepartment of Laboratory, Affiliated Houjie Hospital, Guangdong Medical College, Dongguan, Guangdong 523945, ChinaDepartment of Clinical Laboratory, The Third Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510240, ChinaBackground. Myocardial infarction (MI) is cardiac tissue necrosis caused by acute and persistent ischemic hypoxia of the coronary arteries. This study is aimed at investigating the expression of long noncoding RNA (lncRNA) LINC00261 in MI and its effect on myocardial cells. Methods. qRT-PCR was performed to detect the expression levels of LINC00261, miR-522-3p, and TNRC6A in normal and MI cells. Western blotting analysis was performed to detect the expression of TNRC6A protein. Viability and apoptosis of myocardial cells after MI with the knockout of LINC00261 or TNRC6A were detected. The relationships among miR-522-3p, LINC00261, and TNRC6A in cardiomyocytes were evaluated using a double luciferase reporter gene assay. Hypoxic preconditioning in normal cells was used to construct a simulated MI environment to investigate the effect of LINC00261 on apoptosis of cardiac cells. Results. LINC00261 and TNRC6A were upregulated, while miR-522-3p was downregulated in coronary heart disease tissues with MI. Knockout of LINC00261 can increase the viability of cardiomyocytes and inhibit cell apoptosis. LINC00261 targets miR-522-3p in cardiomyocytes. In addition, miR-522-3p targets TNRC6A in cardiomyocytes. TNRC6A regulates cell viability and apoptosis of cardiomyocytes after MI, and TNRC6A-induced MI can be reversed by overexpression of miR-522-3p. Conclusions. LINC00261 downregulated miR-522-3p in cardiomyocytes after MI by directly targeting miR-522-3p. TNRC6A is the direct target of miR-522-3p. Our results indicated that LINC00261 might serve as a therapeutic target for the treatment of MI.http://dx.doi.org/10.1155/2021/6628194 |
| spellingShingle | Chaoxin Jiang Qing Zhao Chenlong Wang Minyan Peng Guoqing Hao Zhifeng Liu Wenjin Fu Kewei Zhao Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis Cardiovascular Therapeutics |
| title | Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis |
| title_full | Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis |
| title_fullStr | Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis |
| title_full_unstemmed | Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis |
| title_short | Downregulation of Long Noncoding RNA LINC00261 Attenuates Myocardial Infarction through the miR-522-3p/Trinucleotide Repeat-Containing Gene 6a (TNRC6A) Axis |
| title_sort | downregulation of long noncoding rna linc00261 attenuates myocardial infarction through the mir 522 3p trinucleotide repeat containing gene 6a tnrc6a axis |
| url | http://dx.doi.org/10.1155/2021/6628194 |
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