MicroRNA-26b inhibits cardiac remodeling after myocardial infarction by targeting ring finger protein 6 expression
Introduction This study aimed to determine the regulatory mechanism of miR-26b in myocardial infarction (MI)-induced cardiac remodeling through apoptosis. Material and methods An MI rat model was established by left coronary artery ligation. Microarray data were analyzed to distinguish differential...
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| Format: | Article |
| Language: | English |
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Termedia Publishing House
2021-04-01
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| Series: | Archives of Medical Science |
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| Online Access: | https://www.archivesofmedicalscience.com/MicroRNA-26b-inhibits-cardiac-remodeling-after-myocardial-infarction-by-targeting,130649,0,2.html |
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| author | Chun-Mei Tang Qiang Su Hai-Xia Zhao He-Huan Sui Jing Liang Li-Sha Zhu Si-Yun Yang Tao Liu |
| author_facet | Chun-Mei Tang Qiang Su Hai-Xia Zhao He-Huan Sui Jing Liang Li-Sha Zhu Si-Yun Yang Tao Liu |
| author_sort | Chun-Mei Tang |
| collection | DOAJ |
| description | Introduction
This study aimed to determine the regulatory mechanism of miR-26b in myocardial infarction (MI)-induced cardiac remodeling through apoptosis.
Material and methods
An MI rat model was established by left coronary artery ligation. Microarray data were analyzed to distinguish differentially expressed genes in MI. miR-26b was found to be poorly expressed, whereas ring finger protein 6 (RNF6) was highly expressed in MI. Consequently, miR-26b was identified to target RNF6 using dual-luciferase reporter assay and bioinformatics prediction. Furthermore, rats injected with a lentiviral vector expressing miR-26b mimic and/or RNF6 were used to evaluate the role of miR-26b and RNF6 in regulating cardiac function, infarct size, and cardiomyocyte apoptosis.
Results
miR-26b overexpression improved cardiac function and increased left ventricular end-diastolic and end-systolic diameters. Meanwhile, increased miR-26b expression decreased infarct size and cardiomyocyte apoptosis. Moreover, RNF6 overexpression counteracted the role of miR-26b in cardiac function. Additionally, an in vitro cell model illustrated that miR-26b upregulation could increase cell viability and reduce apoptosis, whereas RNF6 overexpression reversed its effect. We also found that the miR-26b mimic could negatively modulate RNF6 expression to inactivate the ERα/Bcl-xL axis.
Conclusions
miR-26b plays a protective role against cardiac remodeling after MI through inactivation of the RNF6/ERα/Bcl-xL axis, supporting miR-26b and RNF6 as potential therapeutic targets for MI. |
| format | Article |
| id | doaj-art-ae29323510594ac7a504880198c79a8d |
| institution | Kabale University |
| issn | 1734-1922 1896-9151 |
| language | English |
| publishDate | 2021-04-01 |
| publisher | Termedia Publishing House |
| record_format | Article |
| series | Archives of Medical Science |
| spelling | doaj-art-ae29323510594ac7a504880198c79a8d2025-01-27T10:45:12ZengTermedia Publishing HouseArchives of Medical Science1734-19221896-91512021-04-012062009202110.5114/aoms/130649130649MicroRNA-26b inhibits cardiac remodeling after myocardial infarction by targeting ring finger protein 6 expressionChun-Mei Tang0Qiang Su1Hai-Xia Zhao2He-Huan Sui3Jing Liang4Li-Sha Zhu5Si-Yun Yang6Tao Liu7Department of Pharmacy, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College (University), Nanchong, Sichuan, ChinaDepartment of Pharmacy, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College (University), Nanchong, Sichuan, ChinaDepartment of Pharmacy, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College (University), Nanchong, Sichuan, ChinaDepartment of Pharmacy, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College (University), Nanchong, Sichuan, ChinaDepartment of Pharmacy, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College (University), Nanchong, Sichuan, ChinaDepartment of Pharmacy, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College (University), Nanchong, Sichuan, ChinaDepartment of Pharmacy, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College (University), Nanchong, Sichuan, ChinaNanchong Key Laboratory of Individualized Drug Therapy, Nanchong, Sichuan, ChinaIntroduction This study aimed to determine the regulatory mechanism of miR-26b in myocardial infarction (MI)-induced cardiac remodeling through apoptosis. Material and methods An MI rat model was established by left coronary artery ligation. Microarray data were analyzed to distinguish differentially expressed genes in MI. miR-26b was found to be poorly expressed, whereas ring finger protein 6 (RNF6) was highly expressed in MI. Consequently, miR-26b was identified to target RNF6 using dual-luciferase reporter assay and bioinformatics prediction. Furthermore, rats injected with a lentiviral vector expressing miR-26b mimic and/or RNF6 were used to evaluate the role of miR-26b and RNF6 in regulating cardiac function, infarct size, and cardiomyocyte apoptosis. Results miR-26b overexpression improved cardiac function and increased left ventricular end-diastolic and end-systolic diameters. Meanwhile, increased miR-26b expression decreased infarct size and cardiomyocyte apoptosis. Moreover, RNF6 overexpression counteracted the role of miR-26b in cardiac function. Additionally, an in vitro cell model illustrated that miR-26b upregulation could increase cell viability and reduce apoptosis, whereas RNF6 overexpression reversed its effect. We also found that the miR-26b mimic could negatively modulate RNF6 expression to inactivate the ERα/Bcl-xL axis. Conclusions miR-26b plays a protective role against cardiac remodeling after MI through inactivation of the RNF6/ERα/Bcl-xL axis, supporting miR-26b and RNF6 as potential therapeutic targets for MI.https://www.archivesofmedicalscience.com/MicroRNA-26b-inhibits-cardiac-remodeling-after-myocardial-infarction-by-targeting,130649,0,2.htmlmyocardial infarctioncardiac remodelingmicrorna-26bring finger protein 6cardiac functionrats |
| spellingShingle | Chun-Mei Tang Qiang Su Hai-Xia Zhao He-Huan Sui Jing Liang Li-Sha Zhu Si-Yun Yang Tao Liu MicroRNA-26b inhibits cardiac remodeling after myocardial infarction by targeting ring finger protein 6 expression Archives of Medical Science myocardial infarction cardiac remodeling microrna-26b ring finger protein 6 cardiac function rats |
| title | MicroRNA-26b inhibits cardiac remodeling after myocardial infarction by targeting ring finger protein 6 expression |
| title_full | MicroRNA-26b inhibits cardiac remodeling after myocardial infarction by targeting ring finger protein 6 expression |
| title_fullStr | MicroRNA-26b inhibits cardiac remodeling after myocardial infarction by targeting ring finger protein 6 expression |
| title_full_unstemmed | MicroRNA-26b inhibits cardiac remodeling after myocardial infarction by targeting ring finger protein 6 expression |
| title_short | MicroRNA-26b inhibits cardiac remodeling after myocardial infarction by targeting ring finger protein 6 expression |
| title_sort | microrna 26b inhibits cardiac remodeling after myocardial infarction by targeting ring finger protein 6 expression |
| topic | myocardial infarction cardiac remodeling microrna-26b ring finger protein 6 cardiac function rats |
| url | https://www.archivesofmedicalscience.com/MicroRNA-26b-inhibits-cardiac-remodeling-after-myocardial-infarction-by-targeting,130649,0,2.html |
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