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Recently, abnormality of yes-associated protein (YAP) has been reported as the pathogenesis of muscle degeneration of DMD; however YAP activity remains unclear in dystrophic heart of DMD. Herein, we investigated YAP activity using disease-specific induced pluripotent stem cell (iPSC) derived cardiomyocytes (CMs) in DMD. DMD-iPSCs were generated from DMD patient with exon 48\u201354 deletion in <jats:italic>DMD<\/jats:italic>, and genome-edited (Ed)-DMD-iPSCs with in-frame (Ed-DMD-iPSCs) were created using CRISPR\/Cas9. Nuclear translocation of YAP [nuclear (N)\/cytoplasmic (C) ratio] was significantly lower in DMD-iPSC-CMs than in Ed-DMD-iPSC-CMs. In addition, Ki67 expression, indicating proliferative ability, was significantly lower in DMD-iPSC-CMs than Ed-DMD-iPSC-CMs. Therefore, immunofluorescent staining showed that actin stress fibers associated with YAP activity by mechanotransduction were disorganized in DMD-iPSC-CMs. Lysophosphatidic acid (LPA), a known lipid mediator on induction of actin polymerization, significantly increased YAP activity and actin dynamics in DMD-iPSC-CMs using live cell imaging. These results suggested that altered YAP activity due to impaired actin dynamics reduced proliferative ability in DMD-iPSC-CMs. Hence, decreased YAP activity in dystrophic heart may contribute to DMD-cardiomyopathy pathogenesis.<\/jats:p>","DOI":"10.1038\/s41598-021-89603-8","type":"journal-article","created":{"date-parts":[[2021,5,14]],"date-time":"2021-05-14T10:03:17Z","timestamp":1620986597000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Decreased YAP activity reduces proliferative ability in human induced pluripotent stem cell of duchenne muscular dystrophy derived cardiomyocytes"],"prefix":"10.1038","volume":"11","author":[{"given":"Hideki","family":"Yasutake","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jong-Kook","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akihito","family":"Hashimoto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kiyoshi","family":"Masuyama","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuki","family":"Kuramoto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuichiro","family":"Higo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shungo","family":"Hikoso","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyoko","family":"Hidaka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Atsuhiko T.","family":"Naito","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shigeru","family":"Miyagawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoshiki","family":"Sawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Issei","family":"Komuro","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yasushi","family":"Sakata","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,5,14]]},"reference":[{"issue":"2","key":"89603_CR1","doi-asserted-by":"publisher","first-page":"291","DOI":"10.1152\/physrev.00028.2001","volume":"82","author":"DJ Blake","year":"2002","unstructured":"Blake, D. J., Weir, A., Newey, S. E. & Davies, K. E. Function and genetics of dystrophin and dystrophin-related proteins in muscle. Physiol. Rev. 82(2), 291\u2013329. https:\/\/doi.org\/10.1152\/physrev.00028.2001 (2002).","journal-title":"Physiol. Rev."},{"issue":"236","key":"89603_CR2","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1126\/scisignal.2002829","volume":"5","author":"RJ Khairallah","year":"2012","unstructured":"Khairallah, R. J. et al. Microtubules underlie dysfunction in duchenne muscular dystrophy. Sci. Signal. 5(236), 1\u201311. https:\/\/doi.org\/10.1126\/scisignal.2002829 (2012).","journal-title":"Sci. Signal."},{"issue":"1","key":"89603_CR3","doi-asserted-by":"publisher","first-page":"153","DOI":"10.1093\/cvr\/cvv021","volume":"106","author":"C Lorin","year":"2015","unstructured":"Lorin, C., V\u00f6geli, I. & Niggli, E. Dystrophic cardiomyopathy: Role of TRPV2 channels in stretch-induced cell damage. Cardiovasc. Res. 106(1), 153\u2013162. https:\/\/doi.org\/10.1093\/cvr\/cvv021 (2015).","journal-title":"Cardiovasc. Res."},{"issue":"5","key":"89603_CR4","doi-asserted-by":"publisher","first-page":"457","DOI":"10.1242\/dmm.019505","volume":"8","author":"Bo Lin","year":"2015","unstructured":"Lin, Bo. et al. Modeling and study of the mechanism of dilated cardiomyopathy using induced pluripotent stem cells derived from individuals with Duchenne muscular dystrophy. DMM Dis. Models Mech. 8(5), 457\u2013466. https:\/\/doi.org\/10.1242\/dmm.019505 (2015).","journal-title":"DMM Dis. Models Mech."},{"issue":"3","key":"89603_CR5","doi-asserted-by":"publisher","first-page":"145","DOI":"10.1136\/jmedgenet-2015-103387","volume":"53","author":"A Aartsma-Rus","year":"2016","unstructured":"Aartsma-Rus, A., Ginjaar, I. B. & Bushby, K. The importance of genetic diagnosis for Duchenne muscular dystrophy. J. Med. 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