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2000
Volume 20, Issue 6
  • ISSN: 1574-888X
  • E-ISSN: 2212-3946

Abstract

Background

encodes a protein that acts as an antagonist to Nodal/TGF-β and Wnt pathways. A mouse knockout (KO) model has shown that this molecule is associated with left-right asymmetry and cardiac development, with its depletion causing heterotaxia and cardiac hyperplasia.

Objective

This study aimed to investigate the molecular mechanisms affected by the depletion of .

Methods

KO and wild-type embryoid bodies (EBs) were used to assess genetic expression with RNA sequencing. To complement the expression results that pointed towards differences in epithelial to mesenchymal transition (EMT), we evaluated migration and cell attachment. Lastly, valve development was investigated, as it was an established model of EMT.

Results

KO EBs progress faster through differentiation. The differences in expression will lead to differences in the expression of genes involved with Notch and Wnt signalling pathways, as well as changes in the expression of genes encoding membrane proteins. Such changes were accompanied by lower migratory rates in KO EBs, as well as higher concentrations of focal adhesions. Within valve development, is expressed in the myocardium underlying future valve sites, and its depletion compromises correct valve structure.

Conclusion

The range of action goes beyond early development. Its absence leads to significantly different expression patterns and defects in EMT and migration. These results have an translation in mouse heart valve development. Knowledge regarding the influence of in EMT and cell transformation allows further understanding of its role in development, or even in some disease contexts, such as congenital heart defects.

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2025-07-01
2026-02-05
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