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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)
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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
Sprache englisch
Veröffentlichungsjahr 2019
HGF-Berichtsjahr 2019
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
Institut(e) Institute of Diabetes and Regeneration Research (IDR)
POF Topic(s) 90000 - German Center for Diabetes Research
30201 - Metabolic Health
Forschungsfeld(er) Helmholtz Diabetes Center
PSP-Element(e) G-501900-231
G-502300-001
DOI 10.1038/s41598-019-48321-y
WOS ID WOS:000481585600014
Scopus ID 85070792105
Erfassungsdatum 2019-09-19
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