RETRACTED ARTICLE: MiR-138-5p exacerbates hypoxia/reperfusion-induced heart injury through the inactivation of SIRT1-PGC
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Inflammation Research
ORIGINAL RESEARCH PAPER
MiR‑138‑5p exacerbates hypoxia/reperfusion‑induced heart injury through the inactivation of SIRT1‑PGC‑1α Cuiping Wang1 · Xia Sun1 · Zhi Qiu1 · Anyong Chen1,2 Received: 25 May 2019 / Revised: 27 June 2019 / Accepted: 8 July 2019 © Springer Nature Switzerland AG 2019
Abstract Objectives A drastic reduction in myocardial cell apoptosis plays a crucial role in the treatment/management of myocardial infarction, a major cardiovascular health challenge confronting the world, especially the Western world. Accumulating evidence indicates that the cardiotoxicity caused by the apoptotic machinery is partly regulated by miRNAs. The aim of this research is to investigate the role of miR-138-5p on hypoxia/reperfusion-induced heart injury. Methods The expression of miR-138-5p was determined in heart tissue from myocardial infarction patients and rats. Rats were transfection with a miR-138-5p inhibitor to silence miR-138-5p. The cardiac function of rats was detected via echocardiography. SIRT1 and PGC-1α expression in cardiac infarction was detected via quantitative Real-time PCR (qPCR) and Western blot analysis, while the TUNEL assay was used to determine myocardial apoptosis. Results Our observations showed that miR-138-5p expression was upregulated after the induction of myocardial infarction. The miR-138-5p inhibitor significantly improved cardiac function, increased the expression of SIRT1 and PGC-1α, and decreased the rate of myocardial apoptosis, whereas siRNA-SIRT1 reversed these protective effects. Conclusions In conclusion, our study demonstrated that miR-138-5p could promote cardiac ischemia injury via inhibition of the silent information regulator 1 and peroxisome proliferator-initiated receptor gamma and coactivator 1 alpha (SIRT1– PGC-1α) axis. Keywords miR-138-5p · Cardiac · Hypoxia/ischemia · SIRT1 · PGC-1α
Introduction Increasing evidence has shown that the myocardium does not suffer sudden and complete permanent damage; rather, initiation and progression of cardiotoxicity takes time. To improve myocardial infarction patients’ treatment/management outcomes, the myocardium must be salvaged within this time frame. MicroRNAs (miRNAs) are endogenous, Responsible Editor: John Di Battista. Cuiping Wang and Xia Sun contributed equally to this work. * Anyong Chen [email protected] 1
Department of Cardiology, Affiliated Hospital of Jining Medical University, Jining 272000, Shandong, People’s Republic of China
Department of Clinical Laboratory, Affiliated Hospital of Jining Medical University, 89 Guhuai Road, Jining 272000, Shandong, People’s Republic of China
2
non-coding, 20- to 23-nucleotide RNAs that regulate a variety of target genes. Increasing evidence has shown that the cardiotoxicity caused by the apoptotic machinery is partly regulated by miRNAs that participate in hypoxia/ reperfusion-induced heart injury. However, the biochemical functions of all the newly discovered miRNAs and their molecular mechanisms/signaling pathways that are involved in hypoxi
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