Serum response factor is required for cell contact maintenance but dispensable for proliferation in visceral yolk sac endothelium.

ABSTRACT:

Background

Endothelial-specific knockout of the transcription factor serum response factor (SRF) results in embryonic lethality by mid-gestation. The associated phenotype exhibits vascular failure in embryos as well as visceral yolk sac (VYS) tissues. Previous data suggest that this vascular failure is caused by alterations in cell-cell and cell-matrix contacts. In the current study, we sought to more carefully address the role of SRF in endothelial function and cell contact interactions in VYS tissues.

Results

Tie2-Cre recombinase-mediated knockout of SRF expression resulted in loss of detectable SRF from VYS mesoderm by E12.5. This loss was accompanied by decreased expression of smooth muscle alpha-actin as well as vascular endothelial cadherin and claudin 5, endothelial-s

SUBMITTER: Holtz ML 

PROVIDER: S-EPMC3065428 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature