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

Rie Saba, Keiko Kitajima, Lucille Rainbow, Silvia Engert, Mami Uemura, Hidekazu Ishida, Ioannis Kokkinopoulos, Yasunori Shintani, Shigeru Miyagawa, Yoshiakira Kanai, Masami Kanai-Azuma, Peter Koopman, Chikara Meno, John Kenny, Heiko Lickert, Yumiko Saga, Ken Suzuki, Yoshiki Sawa, Kenta Yashiro

研究成果: ジャーナルへの寄稿記事

抄録

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.

元の言語英語
記事番号11953
ジャーナルScientific reports
9
発行部数1
DOI
出版物ステータス出版済み - 12 1 2019

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Endocardium
Myocardium
Stem Cells
Embryonic Structures
Mesoderm
Cardiac Myocytes
Genes
Embryonic Development
Vertebrates
Down-Regulation
Cell Proliferation

All Science Journal Classification (ASJC) codes

  • General

これを引用

Endocardium differentiation through Sox17 expression in endocardium precursor cells regulates heart development in mice. / Saba, Rie; Kitajima, Keiko; Rainbow, Lucille; Engert, Silvia; Uemura, Mami; Ishida, Hidekazu; Kokkinopoulos, Ioannis; Shintani, Yasunori; Miyagawa, Shigeru; Kanai, Yoshiakira; Kanai-Azuma, Masami; Koopman, Peter; Meno, Chikara; Kenny, John; Lickert, Heiko; Saga, Yumiko; Suzuki, Ken; Sawa, Yoshiki; Yashiro, Kenta.

:: Scientific reports, 巻 9, 番号 1, 11953, 01.12.2019.

研究成果: ジャーナルへの寄稿記事

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 2019, 'Endocardium differentiation through Sox17 expression in endocardium precursor cells regulates heart development in mice', Scientific reports, 巻. 9, 番号 1, 11953. https://doi.org/10.1038/s41598-019-48321-y
Saba, Rie ; Kitajima, Keiko ; Rainbow, Lucille ; Engert, Silvia ; Uemura, Mami ; Ishida, Hidekazu ; Kokkinopoulos, Ioannis ; Shintani, Yasunori ; Miyagawa, Shigeru ; Kanai, Yoshiakira ; Kanai-Azuma, Masami ; Koopman, Peter ; Meno, Chikara ; Kenny, John ; Lickert, Heiko ; Saga, Yumiko ; Suzuki, Ken ; Sawa, Yoshiki ; Yashiro, Kenta. / Endocardium differentiation through Sox17 expression in endocardium precursor cells regulates heart development in mice. :: Scientific reports. 2019 ; 巻 9, 番号 1.
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abstract = "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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AU - Ishida, Hidekazu

AU - Kokkinopoulos, Ioannis

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AU - Kanai-Azuma, Masami

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