{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,23]],"date-time":"2026-07-23T21:15:53Z","timestamp":1784841353300,"version":"3.55.0"},"reference-count":30,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2014,6,1]],"date-time":"2014-06-01T00:00:00Z","timestamp":1401580800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2014,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Tetralogy of Fallot (<jats:styled-content style=\"fixed-case\">TOF<\/jats:styled-content>) is a complex congenital heart defect and the micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s regulation in <jats:styled-content style=\"fixed-case\">TOF<\/jats:styled-content> development is largely unknown. Herein, we explored the role of mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s in <jats:styled-content style=\"fixed-case\">TOF<\/jats:styled-content>. Among 75 dysregulated mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>s identified from human heart tissues, mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010940 was the most down\u2010regulated one. Interestingly, mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010940 was most highly expressed in normal human right ventricular out\u2010flow tract comparing to other heart chambers. As <jats:styled-content style=\"fixed-case\">TOF<\/jats:styled-content> is caused by altered proliferation, migration and\/or differentiation of the progenitor cells of the secondary heart field, we isolated Sca\u20101<jats:sup>+<\/jats:sup> human cardiomyocyte progenitor cells (h<jats:styled-content style=\"fixed-case\">CMPC<\/jats:styled-content>) for mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010940 function analysis. mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010940 reduction significantly promoted h<jats:styled-content style=\"fixed-case\">CMPC<\/jats:styled-content>s proliferation and inhibited h<jats:styled-content style=\"fixed-case\">CMPC<\/jats:styled-content>s migration. We found that <jats:italic><jats:styled-content style=\"fixed-case\">JARID<\/jats:styled-content>2<\/jats:italic> is an endogenous target regulated by mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010940. Functional analyses showed that <jats:italic><jats:styled-content style=\"fixed-case\">JARID<\/jats:styled-content>2<\/jats:italic> also affected h<jats:styled-content style=\"fixed-case\">CMPC<\/jats:styled-content>s proliferation and migration. Thus, decreased mi<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\u2010940 affects the proliferation and migration of the progenitor cells of the secondary heart field by targeting <jats:italic><jats:styled-content style=\"fixed-case\">JARID<\/jats:styled-content>2<\/jats:italic> and potentially leads to <jats:styled-content style=\"fixed-case\">TOF<\/jats:styled-content> development.<\/jats:p>","DOI":"10.1111\/jcmm.12309","type":"journal-article","created":{"date-parts":[[2014,6,2]],"date-time":"2014-06-02T02:34:52Z","timestamp":1401676492000},"page":"1830-1839","source":"Crossref","is-referenced-by-count":48,"title":["mi<scp>RNA<\/scp>\u2010940 reduction contributes to human Tetralogy of Fallot development"],"prefix":"10.1111","volume":"18","author":[{"given":"Dandan","family":"Liang","sequence":"first","affiliation":[{"name":"Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China East Hospital Tongji University School of Medicine  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