MiR-181a-5p is involved in the cardiomyocytes apoptosis induced by hypoxia–reoxygenation through regulating SIRT1. Issue 7 (2nd July 2020)

• Record Type: Journal Article
• Authors: Qi, Mingxu; He, Li; Ma, Xiaofeng; Li, Zili
• Is Part Of: Bioscience, biotechnology, and biochemistry. Volume 84:Issue 7(2020)
• Page Start: 1353
• Page End: 1361
• Publication Date: 2020-07-02
• Subjects: Hypoxia–reoxygenation -- cardiomyocytes -- apoptosis -- miR-181a-5p -- SIRT1; Biotechnology -- Periodicals; Biochemistry -- Periodicals; 660.6
• DOI: 10.1080/09168451.2020.1750943
• Languages: English
• ISSNs: 0916-8451

Abstract

ABSTRACT: MiR-181a-5p's mechanism in hypoxia–reoxygenation (H/R)-induced cardiomyocytes apoptosis has not been clarified. This study verified that SIRT1 was the target of miR-181a-5p. MiR-181a-5p expression was up-regulated or down-regulated in H/R-induced cardiomyocytes, and SIRT1 was transfected into cells alone or in combination with miR-181a-5p. Cell viability, apoptosis, levels of released lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD), as well as the Bcl-2, Bax, and Caspase 3 levels in treated cells were tested. On the one hand, down-regulated miR-181a-5p promoted cell viability, reduced released LDH and MDA, and increased SOD level in H/R-induced cardiomyocytes. On the other hand, miR-181a-5p inhibited apoptosis and elevated Bcl-2 expression while decreasing the expressions of Bax and Caspase 3 in treated cells, but the effects of miR-181a-5p could be rescued by SIRT1. In conclusion, miR-181a-5p involved in H/R-induced cardiomyocytes apoptosis through regulating SIRT1, which might become a novel direction for related diseases. GRAPHICAL ABSTRACT: uf0001 SIRT1 counteracted the effects of over-expressed miR-181a-5p on hypoxia/reoxygenation (H/R)-induced cardiomyocytes. Abbreviations: H/R: hypoxia–reoxygenation; qRT-PCR: quantitative reverse transcription-polymerase chain reaction; WB: western blot; MDA: malondialdehyde; LDH: lactate dehydrogenase; SOD: superoxide dismutase; AMI: Acute myocardial infarction; I/R: ischemia–reperfusion; DNA: Deoxyribonucleic acid; miRNAs: microRNA; mRNA: messenger RNAs; 3ʹ UTR: 3ʹ-untranslated region; NC: negative control; OD: optical density; PI: propidium iodide; PVDF: polyvinylidene fluoride