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dc.contributor.authorSaba, Rie
dc.contributor.authorKitajima, Keiko
dc.contributor.authorRainbow, Lucille
dc.contributor.authorEngert, Silvia
dc.contributor.authorUemura, Mami
dc.contributor.authorIshida, Hidekazu
dc.contributor.authorKokkinopoulos, Ioannis
dc.contributor.authorShintani, Yasunori
dc.contributor.authorMiyagawa, Shigeru
dc.contributor.authorKanai, Yoshiakira
dc.contributor.authorKanai-Azuma, Masami
dc.contributor.authorKoopman, Peter
dc.contributor.authorMeno, Chikara
dc.contributor.authorKenny, John
dc.contributor.authorLickert, Heiko
dc.contributor.authorSaga, Yumiko
dc.contributor.authorSuzuki, Ken
dc.contributor.authorSawa, Yoshiki
dc.contributor.authorYashiro, Kenta
dc.date.accessioned2020-06-10T16:06:18Z
dc.date.available2020-06-10T16:06:18Z
dc.date.issued2019-08-16
dc.identifier.citationSaba, R., Kitajima, K., Rainbow, L., Engert, S., Uemura, M., Ishida, H., Kokkinopoulos, I., Shintani, Y., Miyagawa, S., Kanai, Y., Kanai-Azuma, M., Koopman, P., Meno, C., Kenny, J., Lickert, H., Saga, Y., Suzuki, K., Sawa, Y. and Yashiro, K. Endocardium differentiation through Sox17 expression in endocardium precursor cells regulates heart development in mice. Scientific Reports, 2019, 9(1). doi: https://doi.org/10.1038/s41598-019-48321-yen_US
dc.identifier.issn2045-2322
dc.identifier.urihttp://hdl.handle.net/11019/1967
dc.descriptionpeer-revieweden_US
dc.description.abstractThe endocardium is the endothelial component of the vertebrate heart and plays a key role in heart development. Where, when, and how the endocardium segregates during embryogenesis have remained largely unknown, however. We now show that Nkx2-5+ cardiac progenitor cells (CPCs) that express the Sry-type HMG box gene Sox17 from embryonic day (E) 7.5 to E8.5 specifically differentiate into the endocardium in mouse embryos. Although Sox17 is not essential or sufficient for endocardium fate, it can bias the fate of CPCs toward the endocardium. On the other hand, Sox17 expression in the endocardium is required for heart development. Deletion of Sox17 specifically in the mesoderm markedly impaired endocardium development with regard to cell proliferation and behavior. The proliferation of cardiomyocytes, ventricular trabeculation, and myocardium thickening were also impaired in a non-cell-autonomous manner in the Sox17 mutant, likely as a consequence of down-regulation of NOTCH signaling. An unknown signal, regulated by Sox17 and required for nurturing of the myocardium, is responsible for the reduction in NOTCH-related genes in the mutant embryos. Our results thus provide insight into differentiation of the endocardium and its role in heart development.en_US
dc.language.isoenen_US
dc.publisherSpringer Science and Business Media LLCen_US
dc.relation.ispartofseriesScientific Reports;Vol. 9 (1)
dc.rightsAttribution-NonCommercial-ShareAlike 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/us/*
dc.subjectSox17en_US
dc.subjectEndocardium differentiationen_US
dc.subjectendocardium precursor cellsen_US
dc.subjectheart developmenten_US
dc.subjectendocardiumen_US
dc.titleEndocardium differentiation through Sox17 expression in endocardium precursor cells regulates heart development in miceen_US
dc.typeArticleen_US
dc.identifier.doi10.1038/s41598-019-48321-y
dc.identifier.doihttps://doi.org/10.1038/s41598-019-48321-y
dc.contributor.sponsorMedical Research Council, U.K.en_US
dc.contributor.sponsorBritish Heart Foundationen_US
dc.contributor.sponsorJapan Society for the Promotion of Science Grants-in-Aid for Scientific Researchen_US
dc.contributor.sponsorGrantNumberG0900105en_US
dc.contributor.sponsorGrantNumberPG/11/102/29213en_US
dc.contributor.sponsorGrantNumber17H04228en_US
dc.contributor.sponsorGrantNumber17K08490en_US
dc.source.volume9
dc.source.issue1
refterms.dateFOA2020-06-10T16:06:18Z


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