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LncRNAMORT is upregulated in myocardial infarction and promotes the apoptosis of cardiomyocyte by downregulating miR-93

Authors
  • Lv, Jing1
  • Zhu, Yi1
  • Yao, Shanglong1
  • 1 Huazhong University of Science and Technology, No.1277 Jiefang Avenue, Wuhan City, Hubei Province, 430000, People’s Republic of China , Wuhan City (China)
Type
Published Article
Journal
BMC Cardiovascular Disorders
Publisher
Springer (Biomed Central Ltd.)
Publication Date
May 25, 2020
Volume
20
Issue
1
Identifiers
DOI: 10.1186/s12872-020-01522-0
Source
Springer Nature
Keywords
License
Green

Abstract

BackgroundMyocardial infarction (MI) affects the expression of a large number of lncRNAs, while the functions of those dysregulated lncRNAs are mostly unclear.Materials and methodsExpression of MORT and miR-93 in hearth tissues and plasma of both MI mice and Sham mice and both MI patients and healthy controls was detected by RT-qPCR. Correlations of expression levels of MORT and miR-93 between hear tissues and plasma of MI mice were explored by performing linear regression.ResultsIn the present study we found that MORT expression levels were higher, while expression levels of miR-93 were lower in both plasma and heart tissues of mice MI mice models compared with Sham mice. Plasma levels of MORT and miR-93 were largely consistent with expression levels of MORT and miR-93 in heart tissue of MI mice. MORT expression levels were also higher, while levels of miR-93 were also lower in plasma of MI patients compared with healthy controls. MORT and miR-93 were inversely correlated in MI patients but not in healthy controls. MORT overexpression resulted in inhibited miR-93 expression in cardiomyocytes (AC16 cell line), while miR-93 overexpression did not significantly affect MORT expression. MORT overexpression promoted cardiomyocyte apoptosis, while miR-93 overexpression played and opposite role and attenuated the effects of MORT overexpression.ConclusionTherefore, lncRNA MORT is upregulated in myocardial infarction and promotes the apoptosis of cardiomyocyte by downregulating miR-93.

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