Semaphorin3f as a cardiomyocyte derived regulator of heart chamber development.

ABSTRACT:

Background

During development a pool of precursors form a heart with atrial and ventricular chambers that exhibit distinct transcriptional and electrophysiological properties. Normal development of these chambers is essential for full term survival of the fetus, and deviations result in congenital heart defects. The large number of genes that may cause congenital heart defects when mutated, and the genetic variability and penetrance of the ensuing phenotypes, reveals a need to understand the molecular mechanisms that allow for the formation of chamber-specific cardiomyocyte differentiation.

Methods

We used in situ hybridization, immunohistochemistry and functional analyses to identify the consequences of the loss of the secreted semaphorin, Sema3fb, in the development of the

SUBMITTER: Halabi R 

PROVIDER: S-EPMC9389736 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature