Exosomes derived from miR‐129‐5p modified bone marrow mesenchymal stem cells represses ventricular remolding of mice with myocardial infarction
Autor: | Liu Li, Yanchun Ren, Shuo Wang, Lei Xu, Jingjie Dong, Xitian Hu, Rubing Wu |
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Rok vydání: | 2021 |
Předmět: |
Myocardial Infarction
Biomedical Engineering Medicine (miscellaneous) Apoptosis Inflammation Exosomes HMGB1 Proinflammatory cytokine Biomaterials Mice Fibrosis microRNA Animals Medicine biology business.industry Myocardium Mesenchymal stem cell Mesenchymal Stem Cells medicine.disease Microvesicles MicroRNAs Cancer research biology.protein medicine.symptom business |
Zdroj: | Journal of Tissue Engineering and Regenerative Medicine. 16:177-187 |
ISSN: | 1932-7005 1932-6254 |
DOI: | 10.1002/term.3268 |
Popis: | Background Myocardial infraction (MI) is a severe disease with great mortality. Mesenchymal stem cells (MSCs)-derived exosomes display protection against MI. MicroRNA-129-5p was reported to exert anti-inflammation activity by targeting high mobility group box 1 (HMGB1). In the present study, the effects of MSCs-derived exosomes overexpressing miR-129-5p on MI were evaluated. Methods Bone marrow mesenchymal stem cells (BMSCs) were transfected with miR-129-5p for exosomes isolation. MI mice model was established and administrated exosomes overexpressing miR-129-5p. The cardiac function, expression of HMGB1,inflammatory cytokines, apoptosis and fibrosis in heart tissues were measured. Resutls MiR-129-5p inhibited HMGB1 expression in BMSCs. MI mice treated with exosomes overexpressing miR-129-5p had enhanced cardiac function and decreased expression of HMGB1 and production of inflammatory cytokines. Exosomes overexpressing miR-129-5p further prevented apoptosis and fibrosis. Conclusion Exosome-mediated transfer of miR-129-5p suppressed inflammation in MI mice by targeting HMGB1. This article is protected by copyright. All rights reserved. |
Databáze: | OpenAIRE |
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