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New candidate genes for ST-elevation myocardial infarction

Journal article
Authors S. Cederstrom
P. Lundman
L. Folkersen
G. Paulsson-Berne
G. Karadimou
P. Eriksson
Kenneth Caidahl
A. Gabrielsen
T. Jernberg
J. Persson
P. Tornvall
Published in Journal of Internal Medicine
ISSN 0954-6820
Publication year 2019
Published at Institute of Medicine, Department of Molecular and Clinical Medicine
Language en
Links dx.doi.org/10.1111/joim.12976
Keywords acute myocardial infarction, atherothrombosis, cardiovascular clinical research, plaque rupture, cholesterol efflux, kappa-b, abcg1, atherosclerosis, expression, receptor, mice, inflammation, deficiency, statins, General & Internal Medicine
Subject categories Clinical Medicine

Abstract

Background Despite extensive research in atherosclerosis, the mechanisms of coronary atherothrombosis in ST-elevation myocardial infarction (STEMI) patients are undetermined. Objectives Our aim was to find candidate genes involved in STEMI by analysing leucocyte gene expression in STEMI patients, without the influence of secondary inflammation from innate immunity, which was assumed to be a consequence rather than the cause of coronary atherothrombosis. Methods Fifty-one patients were included at coronary angiography because of STEMI. Arterial blood was sampled in the acute phase (P1), at 24-48 h (P2) and at 3 months (P3). Leucocyte RNA was isolated and gene expression analysis was performed by Affymetrix Human Transcriptome Array 2.0. By omission of up- or downregulated genes at P2, secondary changes from innate immunity were excluded. Genes differentially expressed in P1 when compared to the convalescent sample in P3 were determined as genes involved in STEMI. Results Three genes were upregulated at P1 compared to P3; ABCG1 (P = 5.81 x 10(-5)), RAB20 (P = 3.69 x 10(-5)) and TMEM2 (P = 7.75 x 10(-6)) whilst four were downregulated; ACVR1 (P = 9.01 x 10(-5)), NFATC2IP (P = 8.86 x 10(-5)), SUN1 (P = 3.87 x 10(-5)) and TTC9C (P = 7.18 x 10(-6)). These genes were also highly expressed in carotid atherosclerotic plaques. Conclusions We found seven genes involved in STEMI. The study is unique regarding the blood sampling in the acute phase and omission of secondary expressed genes from innate immunity. However, the results need to be replicated by future studies.

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