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Saba, 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.* ; Yashiro, K.*

Endocardium differentiation through Sox17 expression in endocardium precursor cells regulates heart development in mice.

Sci. Rep. 9:11953 (2019)
Verlagsversion Forschungsdaten DOI
Open Access Gold
Creative Commons Lizenzvertrag
The 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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Transcription Factor; Cre Recombinase; Notch Pathway; Mouse Embryos; Arterial; Gene; Vasculogenesis; Specification; Progenitors; Endoderm
ISSN (print) / ISBN 2045-2322
e-ISSN 2045-2322
Zeitschrift Scientific Reports
Quellenangaben Band: 9, Heft: 1, Seiten: , Artikelnummer: 11953 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Begutachtungsstatus Peer reviewed