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LncRNA‐MIAT regulates fibrosis in hypertrophic cardiomyopathy (HCM) by mediating the expression of miR‐29a‐3p
Author(s) -
Zhou Jing,
Zhou Yu,
Wang Congxia
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28001
Subject(s) - hypertrophic cardiomyopathy , microrna , fibrosis , transfection , luciferase , real time polymerase chain reaction , biology , gene , medicine , genetics
Aim This study aimed to investigate the molecular mechanism underlying the fibrosis in hypertrophic cardiomyopathy (HCM). Method Quantitative real‐time polymerase chain reaction (qRT‐PCR) was performed to measure the expression of potentially relevant microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) in patients with HCM suffering from fibrosis and patients with HCM free of fibrosis. In addition, the regulatory relationship between lncRNAs and miR‐29a was studied using a luciferase assay. Subsequently, area under the receiver‐operating characteristics (ROC) curve (AUC) analysis was conducted to predict the diagnostic value of myocardial infarction‐associated transcript (MIAT), miR‐29a, H19, and MEG3 in patients with HCM. Finally, the predicted regulatory relationship betwe en miR‐29a and MIAT was validated by transfecting cells with different plasmids. Result miR‐29a and MIAT were differently expressed between the fibrosis (+) HCM group and the fibrosis (−) HCM group, thus establishing a negative relationship between the expression of these two genes. In addition, both MIAT and miR‐29a showed the ability to accurately predict the prognosis in patients with HCM. Furthermore, the luciferase activity of wild‐type MIAT was evidently suppressed in cells transfected with miR‐29a mimics, suggesting that the expression of miR‐29a was apparently downregulated in the presence of MIAT. Conclusion The results obtained in this study collectively indicated that the MIAT might be associated with the development of fibrosis (+) HCM via negatively regulating the expression of miR‐29a.