|作者：||Liu Ketong, Zhao Di, Wang Di|
1Department of Cardiology III, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang, China.
2Department of Cardiology I, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang, China.
3Department of Gastroenterology I, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, Heilongjiang, China.
|刊名：||Bioengineered, 2020, Vol.11 (1), pp.11-18|
|关键词：||COX-2; LINC00528; Myocardial infarction; MiR-143-3p;|
|原始语种摘要：||This study is aimed to explore the roles of LINC00528 in myocardial infarction (MI) progression. Quantitative real-time PCR showed that the expression of LINC00528 and COX-2 was upregulated while miR-143-3p expression was down-regulated in post-MI cells. In function assays, LINC00528 suppression promoted post-MI cells proliferation and reduced cell apoptosis in vitro. In mechanism, LINC00528 interacted with miR-143-3p in post-MI cells. COX-2 served as a target of miR-143-3p in post-MI cells. Besides, LINC00528 inhibition on COX-2 expression and post-MI cells progression could be partially abolished by miR-143-3p inhibitors. Therefore, our findings suggested that LINC00528 exerted its regulatory roles in MI via the miR-143-3p/COX-2 axis, which provided a potential therapeutic target for MI... patients treatment.|