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Expression pattern and signification of Cx43,beta-catenin and Smo in the second heart field / 中国组织工程研究
Article en Zh | WPRIM | ID: wpr-1021654
Biblioteca responsable: WPRO
ABSTRACT

BACKGROUND:

The second heart field is crucial for the development of the embryonic heart.Abnormal development of the second heart field can result in multiple cardiac malformations.After Cx43 gene knockout,reduced formation and proliferation of cells of the second heart field can be observed,but the specific reason remains unclear.

OBJECTIVE:

(1)To determine whether β-catenin,Smo and Cx43 were co-expressed in the second heart field and the endoderm,we observed the expression patterns of these proteins.(2)To explore whether Cx43 interacts with the Wnt/β-catenin pathway or the Shh pathway in the development of the second heart field.

METHODS:

Serial paraffin sections of the mouse embryos at embryonic days 10-12 were selected for immunohistochemical staining,hematoxylin-eosin staining and immunofluorescence staining.The primitive gut of mouse embryos at embryonic day 11 was separated for western blot assay and co-immunoprecipitation. RESULTS AND

CONCLUSION:

(1)Cx43 and Isl1 were co-expressed in some mesenchymal cells on the ventral side of the foregut and dorsal wall of the pericardial cavity of mouse embryos at embryonic days 10-12;Isl1 positive cells increased while Cx43 positive cells increased.(2)Cx43 and β-catenin were co-expressed in the ventral part of the endoderm at embryonic days 10-12.(3)Cx43 and Smo were co-expressed in the endoderm at embryonic days 10-12.(4)The co-immunoprecipitation results confirmed that there was an interaction between Cx43 and β-catenin,which suggested that Cx43 interacted with β-catenin to participate in the development of the second heart field.
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Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Chinese Journal of Tissue Engineering Research Año: 2024 Tipo del documento: Article
Texto completo: 1 Índice: WPRIM Idioma: Zh Revista: Chinese Journal of Tissue Engineering Research Año: 2024 Tipo del documento: Article