Endoglin and Alk5 regulate epithelial-mesenchymal transformation during cardiac valve formation.

ABSTRACT: Endoglin is an accessory receptor for TGFbeta and can associate with Alk5 or Alk2. Although prior studies indicated that endoglin and Alk5 were not directly involved in epithelial-mesenchymal transformation (EMT) in the heart, the expression pattern of endoglin prompted a re-examination. We here show that loss of endoglin expression mediated by either antisense DNA or siRNA results in a direct perturbation of EMT and reduced expression of EMT markers including slug, runx2, RhoA, and latrophilin-2. An examination of BrdU incorporation shows that, while endoglin regulates proliferation at an early stage, reduced endothelial cell proliferation does not account for the loss of mesenchyme. As Alk5 interacts with endoglin, we utilized siRNA and a specific inhibitor, HTS466284 (HTS), to perturb t

SUBMITTER: Mercado-Pimentel ME 

PROVIDER: S-EPMC2001167 | biostudies-literature | 2007 Apr

REPOSITORIES: biostudies-literature