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We sought to identify expression signatures of early MI and subclinical atherosclerosis in the Framingham Heart Study (FHS). In this study, we conducted paired-end RNA sequencing on whole blood collected from 198 FHS participants (55 with a history of early MI, 72 with high CAC without prior MI, and 71 controls free of elevated CAC levels or history of MI). We applied DESeq2 to identify coding-genes and long intergenic noncoding RNAs (lincRNAs) differentially expressed in MI and high CAC, respectively, compared with the control.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>On average, 150 million paired-end reads were obtained for each sample. At the false discovery rate (FDR) &lt;\u20090.1, we found 68 coding genes and 2 lincRNAs that were differentially expressed in early MI versus controls. Among them, 60 coding genes were detectable and thus tested in an independent RNA-Seq data of 807 individuals from the Rotterdam Study, and 8 genes were supported by <jats:italic>p<\/jats:italic> value and direction of the effect. Immune response, lipid metabolic process, and interferon regulatory factor were enriched in these 68 genes. By contrast, only 3 coding genes and 1 lincRNA were differentially expressed in high CAC versus controls. <jats:italic>APOD<\/jats:italic>, encoding a component of high-density lipoprotein, was significantly downregulated in both early MI (FDR\u2009=\u20090.007) and high CAC (FDR\u2009=\u20090.01) compared with controls.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>We identified transcriptomic signatures of early MI that include differentially expressed protein-coding genes and lincRNAs, suggesting important roles for protein-coding genes and lincRNAs in the pathogenesis of MI.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12920-020-00838-2","type":"journal-article","created":{"date-parts":[[2021,2,10]],"date-time":"2021-02-10T08:08:33Z","timestamp":1612944513000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Genome-wide transcriptome study using deep RNA sequencing for myocardial infarction and coronary artery calcification"],"prefix":"10.1186","volume":"14","author":[{"name":"BIOS Consortium","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8237-1857","authenticated-orcid":false,"given":"Xiaoling","family":"Zhang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeroen G. 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Written informed consent was obtained from each enrolled participant.","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and consent to participate"}},{"value":"Not Applicable.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for publication"}},{"value":"The authors declare no competing financial interests.The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services.This work was performed within the framework of the Biobank-Based Integrative Omics Studies (BIOS) Consortium funded by BBMRI-NL, a research infrastructure financed by the Dutch government (NWO 184.021.007). The Rotterdam study is funded by the Erasmus Medical Center and Erasmus University, Rotterdam, Netherlands Organization for the Health Research and development (ZonMw), the Research Institute for Diseases in the Elderly (RIDE), the Ministry of Education, Culture and Science, the ministry for Health, Welfare and Sports, the European Commission (DG XII), and the Municipality of Rotterdam.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"45"}}