Open AccessLong noncoding RNA MIAT: A potential role in the diagnosis and mediation of acute myocardial infarction
Author(s) -
Mayra Azat,
Xiaokelaiti Huojiahemaiti,
Ranran Gao,
Peng Peng
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10768
Subject(s) - myocardial infarction , biomarker , medicine , gene knockdown , cardiology , biology , long non coding rna , apoptosis , rna , gene , biochemistry
The long noncoding RNA myocardial infarction associated transcript (MIAT) has been shown to be a risk allele for myocardial infarction in a previous study. However, there is still controversy about whether MIAT can be used as a biomarker for acute myocardial infarction (AMI). Peripheral blood from patients with AMI and non‑AMI patients was collected to detect the expression levels of MIAT by reverse transcription‑quantitative PCR. Correlation analysis and receiver operating characteristic (ROC) curve analysis were performed to calculate the diagnostic value of MIAT. A rat AMI model was established to detect the expression of MIAT in plasma and cardiac samples. Neonatal rat cardiomyocytes were isolated and exposed to hypoxia, and MIAT small interfering RNAs were transfected into cells to test the expression levels of MIAT and to perform apoptosis‑related assays. The results showed that the plasma levels of MIAT were significantly increased in patients with AMI compared with non‑AMI patients. Correlation analysis showed that MIAT was positively associated with creatine kinase‑MB and cardiac troponin T (cTnT). ROC analysis indicated that MIAT had the same diagnostic value as cTnT. In addition, MIAT was expressed at low levels in the normal rat heart and was highly expressed in AMI hearts. Knockdown of MIAT significantly inhibited cardiomyocyte apoptosis. The present study demonstrated that MIAT may act as a novel potential biomarker for the diagnosis of AMI.