{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,10]],"date-time":"2025-12-10T12:15:17Z","timestamp":1765368917478},"reference-count":44,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2014,4,24]],"date-time":"2014-04-24T00:00:00Z","timestamp":1398297600000},"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":[[2014,7]]},"abstract":"Abstract<\/jats:title>Beta\u2010adrenoceptor (\u03b2\u2010AR<\/jats:styled-content>) exerts critical regulation of cardiac function. MicroRNA<\/jats:styled-content>s (miRNA<\/jats:styled-content>s) are potentially involved in a variety of biological and pathological processes. This study aimed to investigate the role of miRNA<\/jats:styled-content> let\u20107e in the up\u2010regulation of \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> and arrhythmogenesis in acute myocardial infarction (AMI<\/jats:styled-content>) in rats. \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> expression was significantly up\u2010regulated and let\u20107a, c, d, e and i were markedly down\u2010regulated in the infarcted heart after 6 and 24\u00a0hrs myocardial infarction. Forced expression of let\u20107e suppressed \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> expression at the protein level, without affecting \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> mRNA<\/jats:styled-content> level, in neonatal rat ventricular cells (NRVC<\/jats:styled-content>s). Silencing of let\u20107e by let\u20107e antisense inhibitor (AMO<\/jats:styled-content>\u2010let\u20107e) enhanced \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> expression at the protein level in NRVC<\/jats:styled-content>s. Administration of the lentivirus vector containing precursor let\u20107e (len\u2010pre\u2010let\u20107e) significantly inhibited \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> expression in rats, whereas len\u2010AMO<\/jats:styled-content>\u2010let\u20107e up\u2010regulated \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> relative to the baseline control level, presumably as a result of depression of tonic inhibition of \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> by endogenous let\u20107e. Len\u2010negative control (len\u2010NC<\/jats:styled-content>) did not produce significant influence on \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> expression. Len\u2010pre\u2010let\u20107e also profoundly reduced the up\u2010regulation of \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> induced by AMI<\/jats:styled-content> and this effect was abolished by len\u2010AMO<\/jats:styled-content>\u2010let\u20107e. Importantly, len\u2010pre\u2010let\u20107e application significantly reduced arrhythmia incidence after AMI<\/jats:styled-content> in rats and its anti\u2010arrhythmic effect was cancelled by len\u2010AMO<\/jats:styled-content>\u2010let\u20107e. Notably, anti\u2010arrhythmic efficacy of len\u2010pre\u2010let\u20107e was similar to propranolol, a non\u2010selective \u03b2\u2010AR<\/jats:styled-content> blocker and metoprolol, a selective \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> blocker. Down\u2010regulation of let\u20107e contributes to the adverse increase in \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> expression in AMI<\/jats:styled-content> and let\u20107e supplement may be a new therapeutic approach for preventing adverse \u03b21<\/jats:sub>\u2010AR<\/jats:styled-content> up\u2010regulation and treating AMI<\/jats:styled-content>\u2010induced arrhythmia.<\/jats:p>","DOI":"10.1111\/jcmm.12288","type":"journal-article","created":{"date-parts":[[2014,4,24]],"date-time":"2014-04-24T09:39:09Z","timestamp":1398332349000},"page":"1334-1343","source":"Crossref","is-referenced-by-count":18,"title":["let\u20107e replacement yields potent anti\u2010arrhythmic efficacy via<\/i> targeting beta 1\u2010adrenergic receptor in rat heart"],"prefix":"10.1111","volume":"18","author":[{"given":"Xin","family":"Li","sequence":"first","affiliation":[{"name":"Department of Pharmacology (Key Laboratory of Cardiovascular Medicine Research, Ministry of Education; State\u2010Province Key Laboratories of Biomedicine\u2010Pharmaceutics of China) Harbin Medical University Harbin Heilongjiang China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Baoqiu","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pharmacology (Key Laboratory of Cardiovascular Medicine Research, Ministry of Education; State\u2010Province Key Laboratories of Biomedicine\u2010Pharmaceutics of China) Harbin Medical University Harbin Heilongjiang China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hairong","family":"Cui","sequence":"additional","affiliation":[{"name":"Department of Pharmacology (Key Laboratory of Cardiovascular Medicine Research, Ministry of Education; State\u2010Province Key Laboratories of Biomedicine\u2010Pharmaceutics of China) Harbin Medical University Harbin Heilongjiang China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yue","family":"Du","sequence":"additional","affiliation":[{"name":"Department of Pharmacology (Key Laboratory of Cardiovascular Medicine Research, Ministry of Education; State\u2010Province Key Laboratories of Biomedicine\u2010Pharmaceutics of China) Harbin Medical University Harbin Heilongjiang China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yang","family":"Song","sequence":"additional","affiliation":[{"name":"Department of Pharmacology (Key Laboratory of Cardiovascular Medicine Research, Ministry of Education; 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