Key result
MIAT and miR-29a were differentially expressed between fibrosis (+) and fibrosis (-) HCM patients, with MIAT potentially promoting fibrosis by negatively regulating miR-29a expression.
Why the study?
The molecular mechanism underlying fibrosis in hypertrophic cardiomyopathy was not clearly established.
Observational
Answers are grounded in this paper and cite their sources.
Suggests lncRNA-miR-29a involvement in HCM fibrosis; leaves open therapeutic targeting pending validation.
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.
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Zhou et al. (2018) conducted an observational in Hypertrophic cardiomyopathy (HCM). MIAT and miR-29a expression vs. Fibrosis (-) HCM group was evaluated on Expression levels of MIAT and miR-29a and their diagnostic value for fibrosis in HCM. MIAT and miR-29a were differentially expressed between fibrosis (+) and fibrosis (-) HCM patients, with MIAT potentially promoting fibrosis by negatively regulating miR-29a expression.
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