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Micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s (mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s) regulate the development and function of dendritic cells (<jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>s), which are key players in the initiation and regulation of immune responses; however, the underlying regulatory mechanisms remain unclear. Here, we used the supernatants of necrotic primary cardiomyocytes (Necrotic\u2010S) to mimic the myocardial infarction (<jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>) microenvironment to investigate the role of mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s in the regulation of <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content>\u2010mediated inflammatory responses. Our results showed that Necrotic\u2010S up\u2010regulated the <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content> maturation markers <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>40, <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>83 and <jats:styled-content style=\"fixed-case\">CD<\/jats:styled-content>86 and increased the production of inflammatory cytokines, concomitant with the up\u2010regulation of miR\u2010181a and down\u2010regulation of miR\u2010150. Necrotic\u2010S stimulation activated the <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content> pathway and promoted the nuclear translocation of c\u2010Fos and <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03baB p65, and silencing of <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>1 or c\u2010Fos suppressed Necrotic\u2010S\u2010induced <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content> maturation and inflammatory cytokine production. The effects of Necrotic\u2010S on <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content> maturation and inflammatory responses, its activation of the <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content> pathway and the induction of cardiomyocyte apoptosis under conditions of hypoxia were suppressed by miR\u2010181a or miR\u2010150 overexpression. Taken together, these data indicate that miR\u2010181a and miR\u2010150 attenuate <jats:styled-content style=\"fixed-case\">DC<\/jats:styled-content> immune inflammatory responses <jats:italic>via <\/jats:italic><jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>1\u2013<jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>1\/c\u2010Fos signalling and protect cardiomyocytes from cell death under conditions of hypoxia.<\/jats:p>","DOI":"10.1111\/jcmm.13201","type":"journal-article","created":{"date-parts":[[2017,6,9]],"date-time":"2017-06-09T11:24:40Z","timestamp":1497007480000},"page":"2884-2895","source":"Crossref","is-referenced-by-count":67,"title":["miR\u2010181a and miR\u2010150 regulate dendritic cell immune inflammatory responses and cardiomyocyte apoptosis <i>via<\/i> targeting <scp>JAK<\/scp>1\u2013<scp>STAT<\/scp>1\/c\u2010Fos pathway"],"prefix":"10.1111","volume":"21","author":[{"given":"Jianbing","family":"Zhu","sequence":"first","affiliation":[{"name":"Shanghai Institute of Cardiovascular Diseases Zhongshan Hospital Fudan University Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kang","family":"Yao","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Cardiovascular Diseases Zhongshan Hospital Fudan University Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junjie","family":"Guo","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Cardiovascular Diseases Zhongshan Hospital Fudan University Shanghai China"},{"name":"Department of Cardiology The Affiliated Hospital of Qingdao University Qingdao Shandong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hongtao","family":"Shi","sequence":"additional","affiliation":[{"name":"Shanghai Institute of Cardiovascular Diseases Zhongshan Hospital 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