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dc.contributor.author | Maeda, Hideki | en |
dc.contributor.author | Kami, Daisuke | en |
dc.contributor.author | Maeda, Ryotaro | en |
dc.contributor.author | Murata, Yuki | en |
dc.contributor.author | Jo, Jun-Ichiro | en |
dc.contributor.author | Kitani, Tomoya | en |
dc.contributor.author | Tabata, Yasuhiko | en |
dc.contributor.author | Matoba, Satoaki | en |
dc.contributor.author | Gojo, Satoshi | en |
dc.contributor.alternative | 城, 潤一郎 | ja |
dc.date.accessioned | 2020-12-28T04:57:16Z | - |
dc.date.available | 2020-12-28T04:57:16Z | - |
dc.date.issued | 2020-05 | - |
dc.identifier.issn | 1582-1838 | - |
dc.identifier.uri | http://hdl.handle.net/2433/260574 | - |
dc.description.abstract | Acute myocardial infarction is a leading cause of death among single organ diseases. Despite successful reperfusion therapy, ischaemia reperfusion injury (IRI) can induce oxidative stress (OS), cardiomyocyte apoptosis, autophagy and release of inflammatory cytokines, resulting in increased infarct size. In IRI, mitochondrial dysfunction is a key factor, which involves the production of reactive oxygen species, activation of inflammatory signalling cascades or innate immune responses, and apoptosis. Therefore, intercellular mitochondrial transfer could be considered as a promising treatment strategy for ischaemic heart disease. However, low transfer efficiency is a challenge in clinical settings. We previously reported uptake of isolated exogenous mitochondria into cultured cells through co-incubation, mediated by macropinocytosis. Here, we report the use of transactivator of transcription dextran complexes (TAT-dextran) to enhance cellular uptake of exogenous mitochondria and improve the protective effect of mitochondrial replenishment in neonatal rat cardiomyocytes (NRCMs) against OS. TAT-dextran-modified mitochondria (TAT-Mito) showed a significantly higher level of cellular uptake. Mitochondrial transfer into NRCMs resulted in anti-apoptotic capability and prevented the suppression of oxidative phosphorylation in mitochondria after OS. Furthermore, TAT-Mito significantly reduced the apoptotic rates of cardiomyocytes after OS, compared to simple mitochondrial transfer. These results indicate the potential of mitochondrial replenishment therapy in OS-induced myocardial IRI. | en |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Wiley | en |
dc.rights | © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. | en |
dc.subject | cardiomyocytes | en |
dc.subject | ischaemia reperfusion injury | en |
dc.subject | mitochondrial transfer | en |
dc.subject | oxidative stress | en |
dc.subject | transactivator of transcription | en |
dc.title | TAT-dextran-mediated mitochondrial transfer enhances recovery from models of reperfusion injury in cultured cardiomyocytes | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.jtitle | Journal of cellular and molecular medicine | en |
dc.identifier.volume | 24 | - |
dc.identifier.issue | 9 | - |
dc.identifier.spage | 5007 | - |
dc.identifier.epage | 5020 | - |
dc.relation.doi | 10.1111/jcmm.15120 | - |
dc.textversion | publisher | - |
dc.identifier.pmid | 32212298 | - |
dcterms.accessRights | open access | - |
datacite.awardNumber | 26670586 | - |
jpcoar.funderName | 日本学術振興会 | ja |
jpcoar.funderName.alternative | Japan Society for the Promotion of Science (JSPS) | en |
出現コレクション: | 学術雑誌掲載論文等 |
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