| Literature DB >> 31644943 |
Jingjing Rong1, Hongwei Pan1, Jin He1, Yu Zhang1, Yongjun Hu1, Changlu Wang1, Qinghua Fu1, Wenjuan Fan1, Qiongchao Zou1, Le Zhang1, Yi Tang1, Xiang Peng1, Peng Wang1, Yuanyuan Xiang1, Jianqiang Peng1, Zhengyu Liu2, Zhaofen Zheng3.
Abstract
Myocardial ischemia/reperfusion (IR) injury is one of the most prevalent cardiovascular diseases, known for its high mortality and morbidity worldwide. Based on pre-existing evidence, LGALS3 has been found to be closely associated with cardiac diseases. Hence, the objective of our study is to explore the potential function of KCNQ1OT1/microRNA-204-5p (miR-204-5p)/ LGALS3 axis on myocardial IR injury and the underlying mechanism. A myocardial IR injury mouse model was established in vivo and an in vitro cardiomyocyte model was induced by hypoxia/Reoxygenation exposure. Next, gain- and loss-of-function experiments were employed in order to measure the viability and apoptosis of cardiomyocytes and the area of ischemic infarct by CCK-8, TUNEL staining and Evans blue/TTC double staining. LGALS3 was found to be highly expressed in myocardial IR injury. The downregulation of LGALS3 resulted in the alleviation of myocardial IR injury in mouse models. In addition, KCNQ1OT1 could promote the LGALS3 expression by binding to miR-204-5p, which led to aggravated myocardial IR injury. In conclusion, KCNQ1OT1 binds to miR-204-5p to exacerbate myocardial IR injury in mice through the up-regulation of LGALS3, providing a novel insight for myocardial IR injury treatment.Entities:
Keywords: KCNQ1OT1; LGALS3; MicroRNA-204-5p; Myocardial ischemia/reperfusion injury
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Year: 2019 PMID： 31644943 DOI： 10.1016/j.cellsig.2019.109441
Source DB: PubMed Journal: Cell Signal ISSN： 0898-6568 Impact factor: 4.315