Uncovering potential differentially expressed miRNAs and targeted mRNAs in myocardial infarction based on integrating analysis.

Abstract:

:Myocardial infarction (MI) is one of the leading causes of death globally. The aim of the present study was to find valuable microRNAs (miRNAs/miRs) and target mRNAs in order to contribute to our understanding of the pathology of MI. miRNA and mRNA data were downloaded for differential expression analysis. Then, a regulatory network between miRNAs and mRNAs was established, followed by function annotation of target mRNAs. Thirdly, prognosis and diagnostic analysis of differentially methylated target mRNAs were performed. Finally, an in vitro experiment was used to validate the expression of selected miRNAs and target mRNAs. A total of 19 differentially expressed miRNAs and 1,007 differentially expressed mRNAs were identified. Several regulatory interaction pairs between miRNA and mRNAs were identified, such as hsa‑miR‑142‑2p‑long‑chain‑fatty‑acid‑CoA ligase 1 (ACSL1), hsa‑miR‑15a‑3p‑nicotinamide phosphoribosyltransferase (NAMPT), hsa‑miR‑33b‑5p‑regulator of G‑protein signaling 2 (RGS2), hsa‑miR‑17‑3p‑Jun dimerization protein 2 (JDP2), hsa‑miR‑24‑1‑5p‑aquaporin‑9 (AQP9) and hsa‑miR‑34a‑5p‑STAT1/AKT3. Of note, it was demonstrated that ACSL1, NAMPT, RGS2, JDP2, AQP9, STAT1 and AKT3 had diagnostic and prognostic values for patients with MI. In addition, STAT1 was involved in the 'chemokine signaling pathway' and 'Jak‑STAT signaling pathway'. AKT3 was involved in both the 'MAPK signaling pathway' and 'T cell receptor signaling pathway'. Reverse transcription‑quantitative PCR validation of hsa‑miR‑142‑3p, hsa‑miR‑15a‑3p, hsa‑miR‑33b‑5p, ACSL1, NAMPT, RGS2 and JDP2 expression was consistent with the bioinformatics analysis. In conclusion, the identified miRNAs and mRNAs may be involved in the pathology of MI.

journal_name

Mol Med Rep

authors

Wang S,Cao N

doi

10.3892/mmr.2020.11517

subject

Has Abstract

pub_date

2020-11-01 00:00:00

pages

4383-4395

issue

5

eissn

1791-2997

issn

1791-3004

journal_volume

22

pub_type

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