Circ-RHOJ.1 regulated myocardial cell proliferation and apoptosis via targeting the miR-124-3p/NRG-1 axis in myocardial ischemia/reperfusion injury
Introduction Myocardial ischemia/reperfusion (I/R) injury is a leading cause of cardiac dysfunction. Circular RNAs (circRNAs) are involved in the pathogenesis of myocardial I/R injury. However, the functions and underlying mechanisms are unclear. The present study determined the role of circ-RHOJ.1...
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Termedia Publishing House
2019-08-01
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Series: | Archives of Medical Science |
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Online Access: | https://www.archivesofmedicalscience.com/Circ-RHOJ-1-regulated-myocardial-cell-proliferation-nand-apoptosis-via-targeting,109684,0,2.html |
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author | Yan Liu Xiao Ke Wenyu Guo Xiaoqing Wang Changnong Peng Zhiyong Liao Qiang Liu Yingling Zhou |
author_facet | Yan Liu Xiao Ke Wenyu Guo Xiaoqing Wang Changnong Peng Zhiyong Liao Qiang Liu Yingling Zhou |
author_sort | Yan Liu |
collection | DOAJ |
description | Introduction
Myocardial ischemia/reperfusion (I/R) injury is a leading cause of cardiac dysfunction. Circular RNAs (circRNAs) are involved in the pathogenesis of myocardial I/R injury. However, the functions and underlying mechanisms are unclear. The present study determined the role of circ-RHOJ.1 in regulating myocardial cell proliferation and apoptosis after I/R injury.
Material and methods
Myocardial cells isolated from Sprague-Dawley rats were identified with an immunofluorescence assay using cardiac troponin T antibody. Expression of circ-RHOJ.1, miR-124-3p and neuregulin-1 (NRG1) mRNA was assessed with real-time quantitative polymerase chain reaction. NRG1 protein expression was evaluated with western blot and immunofluorescence assays. Dual-luciferase reporter assay was performed to confirm interaction between miR-124-3p and circ-RHOJ.1, and miR-124-3p and NRG1. Effects of circ-RHOJ.1 overexpression or miR-124-3p inhibition on cell proliferation and apoptosis were evaluated using cell counting kit (CCK)-8 assay and flow cytometry. Cytokines levels were analyzed with an enzyme-linked immunosorbent assay.
Results
Myocardial cells were successfully isolated and had down-regulated expression of circ-RHOJ.1 and NRG1, and up-regulated expression of miR-124-3p after I/R injury. circ-RHOJ.1 acted as a sponge for miR-124-3p, and NRG1 served as a target gene of miR-124-3p. circ-RHOJ.1 overexpression or miR-124-3p inhibition increased interleukin (IL)-10 levels and reduced IL-2, IL-6, and tumor necrosis factor-a levels in myocardial cells after I/R injury. Functional assay results illustrated that circ-RHOJ.1 overexpression or miR-124-3p inhibition enhanced proliferation and inhibited apoptosis of myocardial cells after I/R injury.
Conclusions
Circ-RHOJ.1 served as a molecular marker of myocardial I/R injury via regulation of miR-124-3p and NRG1 expression. |
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language | English |
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spelling | doaj.art-617e81ca555a46748399967fde398bfa2022-12-22T03:24:50ZengTermedia Publishing HouseArchives of Medical Science1734-19221896-91512019-08-0118373274510.5114/aoms.2019.87205109684Circ-RHOJ.1 regulated myocardial cell proliferation and apoptosis via targeting the miR-124-3p/NRG-1 axis in myocardial ischemia/reperfusion injuryYan Liu0Xiao Ke1Wenyu Guo2Xiaoqing Wang3Changnong Peng4Zhiyong Liao5Qiang Liu6Yingling Zhou7Southern Medical University, Guangzhou, ChinaDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Sun Yat-sen Cardiovascular Hospital, Shenzhen, ChinaDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Sun Yat-sen Cardiovascular Hospital, Shenzhen, ChinaDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Sun Yat-sen Cardiovascular Hospital, Shenzhen, ChinaDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Sun Yat-sen Cardiovascular Hospital, Shenzhen, ChinaDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Sun Yat-sen Cardiovascular Hospital, Shenzhen, ChinaDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Sun Yat-sen Cardiovascular Hospital, Shenzhen, ChinaSouthern Medical University, Guangzhou, ChinaIntroduction Myocardial ischemia/reperfusion (I/R) injury is a leading cause of cardiac dysfunction. Circular RNAs (circRNAs) are involved in the pathogenesis of myocardial I/R injury. However, the functions and underlying mechanisms are unclear. The present study determined the role of circ-RHOJ.1 in regulating myocardial cell proliferation and apoptosis after I/R injury. Material and methods Myocardial cells isolated from Sprague-Dawley rats were identified with an immunofluorescence assay using cardiac troponin T antibody. Expression of circ-RHOJ.1, miR-124-3p and neuregulin-1 (NRG1) mRNA was assessed with real-time quantitative polymerase chain reaction. NRG1 protein expression was evaluated with western blot and immunofluorescence assays. Dual-luciferase reporter assay was performed to confirm interaction between miR-124-3p and circ-RHOJ.1, and miR-124-3p and NRG1. Effects of circ-RHOJ.1 overexpression or miR-124-3p inhibition on cell proliferation and apoptosis were evaluated using cell counting kit (CCK)-8 assay and flow cytometry. Cytokines levels were analyzed with an enzyme-linked immunosorbent assay. Results Myocardial cells were successfully isolated and had down-regulated expression of circ-RHOJ.1 and NRG1, and up-regulated expression of miR-124-3p after I/R injury. circ-RHOJ.1 acted as a sponge for miR-124-3p, and NRG1 served as a target gene of miR-124-3p. circ-RHOJ.1 overexpression or miR-124-3p inhibition increased interleukin (IL)-10 levels and reduced IL-2, IL-6, and tumor necrosis factor-a levels in myocardial cells after I/R injury. Functional assay results illustrated that circ-RHOJ.1 overexpression or miR-124-3p inhibition enhanced proliferation and inhibited apoptosis of myocardial cells after I/R injury. Conclusions Circ-RHOJ.1 served as a molecular marker of myocardial I/R injury via regulation of miR-124-3p and NRG1 expression.https://www.archivesofmedicalscience.com/Circ-RHOJ-1-regulated-myocardial-cell-proliferation-nand-apoptosis-via-targeting,109684,0,2.htmlcirc-rhoj.1mir-124-3pneuregulin 1myocardial ischemia/reperfusion injuryproliferationapoptosis |
spellingShingle | Yan Liu Xiao Ke Wenyu Guo Xiaoqing Wang Changnong Peng Zhiyong Liao Qiang Liu Yingling Zhou Circ-RHOJ.1 regulated myocardial cell proliferation and apoptosis via targeting the miR-124-3p/NRG-1 axis in myocardial ischemia/reperfusion injury Archives of Medical Science circ-rhoj.1 mir-124-3p neuregulin 1 myocardial ischemia/reperfusion injury proliferation apoptosis |
title | Circ-RHOJ.1 regulated myocardial cell proliferation
and apoptosis via targeting the miR-124-3p/NRG-1 axis
in myocardial ischemia/reperfusion injury |
title_full | Circ-RHOJ.1 regulated myocardial cell proliferation
and apoptosis via targeting the miR-124-3p/NRG-1 axis
in myocardial ischemia/reperfusion injury |
title_fullStr | Circ-RHOJ.1 regulated myocardial cell proliferation
and apoptosis via targeting the miR-124-3p/NRG-1 axis
in myocardial ischemia/reperfusion injury |
title_full_unstemmed | Circ-RHOJ.1 regulated myocardial cell proliferation
and apoptosis via targeting the miR-124-3p/NRG-1 axis
in myocardial ischemia/reperfusion injury |
title_short | Circ-RHOJ.1 regulated myocardial cell proliferation
and apoptosis via targeting the miR-124-3p/NRG-1 axis
in myocardial ischemia/reperfusion injury |
title_sort | circ rhoj 1 regulated myocardial cell proliferation and apoptosis via targeting the mir 124 3p nrg 1 axis in myocardial ischemia reperfusion injury |
topic | circ-rhoj.1 mir-124-3p neuregulin 1 myocardial ischemia/reperfusion injury proliferation apoptosis |
url | https://www.archivesofmedicalscience.com/Circ-RHOJ-1-regulated-myocardial-cell-proliferation-nand-apoptosis-via-targeting,109684,0,2.html |
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