{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T02:30:51Z","timestamp":1792031451508,"version":"4.4.0"},"reference-count":48,"publisher":"SAGE Publications","license":[{"start":{"date-parts":[[2022,1,1]],"date-time":"2022-01-01T00:00:00Z","timestamp":1640995200000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Hum Exp Toxicol"],"published-print":{"date-parts":[[2022,1]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Bone marrow mesenchymal stem cells (BMMSCs) exert protective effects against myocardial infarction (MI). Here, we focused on the function and mechanism of miR-455-3p from BMMSCs-derived exosomes (BMMSCs-Exo) in myocardial infarction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and methods<\/jats:title>\n                    <jats:p>BMMSCs were isolated from rat bone marrow, and the exosomes from the culture medium of BMMSCs were separated, and administered to H9C2 cells under hypoxia-reperfusion (H\/R) stimulation. MTT and TUNEL staining analyzed cell viability and apoptosis, respectively. RT-qPCR determined miR-455-3p expression. Apoptosis-related proteins, autophagy-associated proteins, and the MEKK1-MKK4-JNK signaling pathway were detected. The interaction between miR-455-3p and MEKK1 was confirmed through dual luciferase activity and RIP assay. An in vivo ischemia reperfusion (I\/R) model was established in rats. 2, 3, 5 triphenyltetrazolium chloride (TTC) staining, hematoxylin-eosin (H&amp;E) staining, Masson staining, and TUNEL staining evaluated the infarct volume and histopathological changes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>miR-455-3p\u2032s expression was down-regulated in BMMSCs-derived exosomes, I\/R myocardial tissues, and H\/R myocardial cells. miR-455-3p enriched by BMMSC exosomes reduced H\/R-mediated cardiomyocyte damage and death-related autophagy. miR-455-3p upregulation suppressed MEKK1-MKK4-JNK. MEKK1 overexpression notably mitigated cell apoptosis, cramped cell viability, suppressed autophagy expansion, and attenuated Exo-miR-455-3p\u2032s protection on H\/R myocardial cells. In-vivo trials reflected that BMMSC exosomes enriched with miR-455-3p repressed ischemia reperfusion-induced myocardial damage and myocardial cell function.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>miR-455-3p, shuttled by exosomes from MSCs, targets the MEKK1-MKK4-JNK signaling pathway to guard against myocardial ischemia-reperfusion damage.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/09603271221102508","type":"journal-article","created":{"date-parts":[[2022,5,18]],"date-time":"2022-05-18T17:28:30Z","timestamp":1652894910000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":38,"title":["Exosomal miR-455-3p from BMMSCs prevents cardiac ischemia-reperfusion injury"],"prefix":"10.1177","volume":"41","author":[{"given":"Yue","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Cardiology, Sinopharm Dongfeng General Hospital, Hubei University of Medicine, Shiyan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7793-6059","authenticated-orcid":false,"given":"Yusi","family":"Shen","sequence":"additional","affiliation":[{"name":"Second Department of Orthopedic Rehabilitation, Taihe Hospital, Hubei University of Medicine, Shiyan, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2022,5,16]]},"reference":[{"key":"bibr1-09603271221102508","doi-asserted-by":"publisher","DOI":"10.1007\/s12013-015-0553-4"},{"key":"bibr2-09603271221102508","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2007.09.011"},{"key":"bibr3-09603271221102508","doi-asserted-by":"publisher","DOI":"10.1161\/STROKEAHA.115.008097"},{"key":"bibr4-09603271221102508","first-page":"14","volume":"206","author":"Ahmadi A","year":"2015","journal-title":"Int J Prev 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