{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T13:18:52Z","timestamp":1789651132887,"version":"4.0.0"},"reference-count":33,"publisher":"American Physiological Society","issue":"8","funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China (NSFC)","doi-asserted-by":"publisher","award":["91442108"],"award-info":[{"award-number":["91442108"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China (NSFC)","doi-asserted-by":"publisher","award":["81000088"],"award-info":[{"award-number":["81000088"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002855","name":"Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology)","doi-asserted-by":"publisher","award":["2013ZX10004609"],"award-info":[{"award-number":["2013ZX10004609"]}],"id":[{"id":"10.13039\/501100002855","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2015,10]]},"abstract":"<jats:p> A growing number of studies have suggested microRNAs (miRNAs) are involved in the modulation of myocardial ischemia-reperfusion (MI\/R) injury; however, the role of endogenous miRNAs targeting endothelial cells (ECs) and its interaction with ICAM-1 in the setting of MI\/R remain poorly understood. Our microarray results showed that miR-146a, miR-146b-5p, miR-155*, miR-155, miR-497, and miR-451 were significantly upregulated, whereas, miR-141 and miR-564 were significantly downregulated in the ECs challenged with TNF-\u03b1 for 6 h. Real-time PCR analyses additionally validated that the expression levels of miR-146a, miR-155*, and miR-141 were consistent with the microarray results. Then, ICAM-1 was identified as a novel target of miR-141 by Target Scan software and the reporter gene system. Further functional experiments showed that elevated levels of miR-141 inhibited ICAM-1 expression and diminished leukocytes adhesion to ECs in vitro. In an in vivo murine model of MI\/R injury, pretreatment with miR-141 mimics through the tail vein downregulated the expression level of ICAM-1 in heart and attenuated MI\/R injury as evidenced by decreased infarct size and decline of serum cardial troponin I (cTnI) and lactate dehydrogenase (LDH) concentration. The cardioprotective effects of miR-141 mimics may be attributed to the decreased infiltration of CD11b<jats:sup>+<\/jats:sup> cells and F4\/80<jats:sup>+<\/jats:sup> macrophages into ischemic myocardium tissue. In conclusion, our results demonstrate that miR-141, as a novel repressor of ICAM-1, is involved in the attenuation of MI\/R injury via antithetical regulation of ICAM-1 and inflammatory cells infiltration. Thus miR-141 may constitute a new therapeutic target in the setting of ischemic heart disease. <\/jats:p>","DOI":"10.1152\/ajpheart.00290.2015","type":"journal-article","created":{"date-parts":[[2015,9,14]],"date-time":"2015-09-14T21:50:13Z","timestamp":1442267413000},"page":"H1303-H1313","source":"Crossref","is-referenced-by-count":60,"title":["MicroRNA-141 regulates the expression level of ICAM-1 on endothelium to decrease myocardial ischemia-reperfusion injury"],"prefix":"10.1152","volume":"309","author":[{"given":"Rong Rong","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Immunology, Fourth Military Medical University, Xi'an, People's Republic of China;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Physiology, Fourth Military Medical University, Xi'an, People's Republic of China;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiu 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