Downregulated LINC01614 Ameliorates Hypoxia/Reoxygenation-Stimulated Myocardial Injury by Directly Sponging microRNA-138-5p

Jie Yang; Xue-Song Yang; Qian Zhang; Xin Zhuang; Xiao-Kang Dong; Yue-Hua Jiang; Yan-Nan Tao; Chuan-Hua Yang

doi:10.1177/1559325820913786

Downregulated LINC01614 Ameliorates Hypoxia/Reoxygenation-Stimulated Myocardial Injury by Directly Sponging microRNA-138-5p

Dose Response. 2020 Mar 20;18(1):1559325820913786. doi: 10.1177/1559325820913786. eCollection 2020 Jan-Mar.

Authors

Jie Yang^{1

2}, Xue-Song Yang³, Qian Zhang⁴, Xin Zhuang², Xiao-Kang Dong², Yue-Hua Jiang⁵, Yan-Nan Tao⁶, Chuan-Hua Yang²

Affiliations

¹ First Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, Shandong, People's Republic of China.
² Department of Cardiovascular, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, People's Republic of China.
³ Department of Vascular Surgery, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, People's Republic of China.
⁴ Department of Science and Technology Office, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, People's Republic of China.
⁵ Central Laboratory, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, People's Republic of China.
⁶ College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, Shandong, People's Republic of China.

Abstract

Background: LINC01614 was abnormally expressed in myocardial infarction and other heart failures. We attempted to detect the effects of LINC01614 in myocardial ischemia-reperfusion (I/R) injury.

Methods: H9c2 cardiomyocyte cells were treated with hypoxia/reoxygenation (H/R) to establish myocardial ischemia (MI) model.

Results: Clinical data of Gene Expression Omnibus (GEO) database indicated that LINC01614 was highly regulated in first acute myocardial infarction, whereas miR-138-5p was downregulated in unstable angina pectoris. LINC01614 inhibition promoted cell proliferation and repressed the apoptotic property after H/R treatment using Cell Counting Kit-8 and flow cytometry analysis. Downregulation of LINC01614 enhanced the expression of Bcl-2 but attenuated Bax and cleaved caspase 3 expression after H/R treatment. Bioinformatics prediction and dual-luciferase reporter assay determined that LINC01614 directly targeted miR-138-5p and negatively regulated the expression of miR-138-5p. Furthermore, the overexpression of miR-138-5p significantly strengthened the function of si-LINC01614 in H/R groups.

Conclusion: Our results illustrated that reduction in LINC01614 attenuated H/R treatment-induced myocardial damage via sponging miR-138-5p.

Keywords: LINC01614; cell behaviors; hypoxia/reoxygenation; miR-138-5p; myocardial ischemia.