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Investigating the Expression Level of MiR-17-3p, MiR-101-3p, MiR-335-3p, and MiR-296-3p in the Peripheral Blood of Patients with Acute Myocardial Infarction

Overview
Publisher Springer
Specialty Biochemistry
Date 2023 May 24
PMID 37222878
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Abstract

The role of inflammation has been proven in acute myocardial infarction (AMI) pathogenesis. Due to the effect of NLRP3 gene expression in the inflammation process of MI, we aimed to explore the expression changes and diagnostic power of four inflammation-related miRNAs including miR-17-3p, miR-101-3p, miR-335-3p, miR-296-3p and their potential target, NLRP3, in ST-segment elevation myocardial infarction (STEMI), and non-STEMI (NSTEMI) patients as two major classes of AMI. The expression level of these genes were evaluated in 300 participants equally divided into three groups of STEMI, NSTEMI, and control using quantitative real-time PCR. The expression level of NLRP3 was upregulated in STEMI and NSTEMI patients compared to control subjects. Besides, the expression levels of miR-17-3p, miR-101-3p, and miR-296-3p were significantly downregulated in STEMI and NSTEMI patients compared to controls. The increased expression of NLRP3 had a very strong inverse correlation with miR-17-3p in patients with STEMI and with miR-101-3p in the STEMI and NSTEMI patients. ROC curve analysis showed that the expression level of miR-17-3p had the highest diagnostic power for discrimination between STEMI patients and controls. Remarkably, the combination of all markers resulted in a higher AUC. In summary, there is a significant association between the expression levels of miR-17-3p, miR-101-3p, miR-335-3p, miR-296-3p, and NLRP3 and the incidence of AMI. Although the miR-17-3p expression level has the highest diagnostic power to distinguish between STEMI patients and control subjects, the combination of these miRNAs and NLRP3 could serve as a novel potential diagnostic biomarker of STEMI.

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References
1.
Anderson J, Morrow D . Acute Myocardial Infarction. N Engl J Med. 2017; 376(21):2053-2064. DOI: 10.1056/NEJMra1606915. View

2.
Bhatt D, Lopes R, Harrington R . Diagnosis and Treatment of Acute Coronary Syndromes: A Review. JAMA. 2022; 327(7):662-675. DOI: 10.1001/jama.2022.0358. View

3.
Daga L, Kaul U, Mansoor A . Approach to STEMI and NSTEMI. J Assoc Physicians India. 2012; 59 Suppl:19-25. View

4.
de Bliek E . ST elevation: Differential diagnosis and caveats. A comprehensive review to help distinguish ST elevation myocardial infarction from nonischemic etiologies of ST elevation. Turk J Emerg Med. 2018; 18(1):1-10. PMC: 6009807. DOI: 10.1016/j.tjem.2018.01.008. View

5.
Feinberg M, Moore K . MicroRNA Regulation of Atherosclerosis. Circ Res. 2016; 118(4):703-20. PMC: 4762069. DOI: 10.1161/CIRCRESAHA.115.306300. View