{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T18:12:38Z","timestamp":1771956758508,"version":"3.50.1"},"reference-count":38,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2018,4,25]],"date-time":"2018-04-25T00:00:00Z","timestamp":1524614400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2018,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>MicroRNAs (miRs) are widely reported to be novel biomarkers involved in the process of coronary atherosclerosis (CAS). Hence, this study aims to explore the function of miR\u2010383\u20103p targeting IL1R2 on inflammatory injury of coronary artery endothelial cells (CAECs) in CAS. The underlying regulatory mechanisms of miR\u2010383\u20103p were analyzed in concert with the treatment of miR\u2010383\u20103p mimics, miR\u2010383\u20103p inhibitors, and the combination of miR\u2010383\u20103p inhibitors and siRNA against IL1R2 in homocysteine (HCY)\u2010induced CAECs. MTT, Hoechst 33258 staining, and tube formation assay were employed in order to measure cell viability, apoptosis, and tube formation, respectively. The levels of IL\u20101\u03b2, IL\u20106, IL\u201010, and IL\u201018 were determined by ELISA. IL1R2 was verified as the target gene of miR\u2010383\u20103p by dual\u2010luciferase reporter gene assay. MiR\u2010383\u20103p was down\u2010regulated in myocardial tissues of AS rats while IL1R2 was the reciprocal. The up\u2010regulation of miR\u2010383\u20103p decreased the levels of IL1R2, caspase\u20101, IL\u20101\u03b2, IL\u20106, and IL\u201018 expressions, as well as cell apoptosis rate in the HCY\u2010induced CAECs, while IL\u201010 expression, cell viability, and tube formation ability were increased. These results were contraindicated in the HCY\u2010induced CAECs treated by miR\u2010383\u20103p inhibitors. In conclusion, miR\u2010383\u20103p mediating IL1R2 prevents HCY\u2010induced apoptosis and inflammation injury in CAECs through the inhibition of the activation of inflammasome signaling pathway. These findings highly indicate that miR\u2010383\u20103p may be beneficial in the prevention of CAS and other cardiovascular diseases.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.26854","type":"journal-article","created":{"date-parts":[[2018,4,25]],"date-time":"2018-04-25T11:13:52Z","timestamp":1524654832000},"page":"6684-6694","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["<i>Retracted<\/i>: The anti\u2010inflammatory effect of microRNA\u2010383\u20103p interacting with IL1R2 against homocysteine\u2010induced endothelial injury in rat coronary arteries"],"prefix":"10.1002","volume":"119","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1672-3364","authenticated-orcid":false,"given":"Zheng","family":"Lian","sequence":"first","affiliation":[{"name":"The First Department of Cardiovascular Medicine Cangzhou Central Hospital Cangzhou Hebei Province P. R. 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