Dataset Information

Identification of lncRNA competitively regulated subpathways in myocardial infarction.

ABSTRACT: The functions of long non-coding RNAs (lncRNAs) in myocardial infarction (MI) remain largely unknown. Thus, we used the subp athway-LINCE method to characterize the potential roles of lncRNAs in MI. Candidate lncRNA-mRNA interactions were obtained from miRNA-mRNA interactions and lncRNA-miRNA interactions. Then the lncRNA and mRNA co-expression relationship pairs (LncGenePairs) were screened from the lncRNAs and mRNA intersections, which were extracted through candidate lncRNA-mRNA interactions and sample gene expression profiles. The lncRNAs in LncGenePairs were embedded into pathway graphs as nodes through linking to their regulated mRNAs, which resulted in obtaining condition-specific lncRNA competitively regulated signal pathways (csLncRPs). Finally, the csLncRPs were calculated using lenient distance similarity to obtain the lncRNA competitively regulated subpathways. Based on the statistical significance of signal subpathways, lncRNA-mRNA networks were constructed, in which hub lncRNAs were selected. A total of 65 lncRNAs competitively regulated subpathways and 13 hub lncRNAs were obtained, which associated with a risk of MI. Identifying lncRNAs competitively regulated subpathways not only provides potential lncRNA biomarkers for MI, but also helps the understanding of pathogenesis of MI.

SUBMITTER: Wu X

PROVIDER: S-EPMC6434249 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Identification of lncRNA competitively regulated subpathways in myocardial infarction.

Wu Xia X Sun Lili L Wang Ziliang Z

Experimental and therapeutic medicine 20190226 4

The functions of long non-coding RNAs (lncRNAs) in myocardial infarction (MI) remain largely unknown. Thus, we used the subp athway-LINCE method to characterize the potential roles of lncRNAs in MI. Candidate lncRNA-mRNA interactions were obtained from miRNA-mRNA interactions and lncRNA-miRNA interactions. Then the lncRNA and mRNA co-expression relationship pairs (LncGenePairs) were screened from the lncRNAs and mRNA intersections, which were extracted through candidate lncRNA-mRNA interactions ...[more]

PMID: 30936975

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Project description:BackgroundPreclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans.Methods and resultsOverall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P<0.0001) and plasma C-reactive protein concentrations (6.50 [2.00 to 12.75] versus 2.00 [0.50 to 4.00] mg/dL, P=0.0005) despite having similar aortic (P=0.12) and less coronary (P=0.006) atherosclerotic burden and similar paraspinal muscular 18F-fluorodeoxyglucose uptake (P=0.52). Patients with ST-segment elevation MI had larger infarcts (peak plasma troponin 32 300 [10 200 to >50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non-ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI.ConclusionsThe presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization: MI begets MI.Clinical trial registrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254.

Dataset Information

Identification of lncRNA competitively regulated subpathways in myocardial infarction.

Publications

Identification of lncRNA competitively regulated subpathways in myocardial infarction.

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