Endoderm contributes to endocardial composition during cardiogenesis

Li, Yan, Wang, Xiaoyu, Ma, Zhenglai, Chuai, Manli, Munsterberg, Andrea ORCID: https://orcid.org/0000-0002-4577-4240, Lee, Kenneth KaHo and Yang, Xuesong (2014) Endoderm contributes to endocardial composition during cardiogenesis. Chinese Science Bulletin, 59 (22). pp. 2749-2755. ISSN 1861-9541

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Abstract

Heart formation commences from a single heart tube, which fuses from bilateral primordial heart fields. The developing heart tube is composed of outer-layer myocardial cells and inner-layer endocardial cells. Several distinct populations of precardiac cells contribute to cardiac morphogenesis. However, it still remains not very clear about the lineage of endocardium at gastrulation stage. Thereby, this study focused on ascertaining the correlation between the hypoblast in gastrulation and endocardium during cardiogenesis. Firstly, the fusing heart tube morphologically is closed to endoderm-derived pharynx floor, implying the possibility that pharynx floor might be wrapped into the formation of endoderm. Secondly, HNK1 is expressed in hypoblast strongly at gastrula stage and subsequently appeared in endocardium of cardiogenesis. Moreover, fate map data displayed that DiI labeled hypoblast was also present in endocardium later on. One more evidence is chick-quail chimera of hypoblast transplantation, in which quail-hypoblast derivative could be identified in endocardium of cardiogenesis by QCPN antibody. In sum, our current data suggests that endoderm in gastrula contribute at least partly to the formation of endocardium of cardiogenesis.

Item Type:	Article
Uncontrolled Keywords:	hypoblast,endoderm,endocardium,dil,fate map,qcpn,quail,chick
Faculty \ School:	Faculty of Science > School of Biological Sciences
UEA Research Groups:	Faculty of Science > Research Groups > Cells and Tissues
Depositing User:	Pure Connector
Date Deposited:	02 Jan 2015 11:58
Last Modified:	18 Apr 2023 21:35
URI:	https://ueaeprints.uea.ac.uk/id/eprint/51591
DOI:	10.1007/s11434-014-0366-7

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