Interaction and Functional Interplay Between Endoglin and ALK-1, Two Components of the Endothelial Transforming Growth Factor-beta Receptor Complex

Overview

Journal J Cell Physiol

Specialties Cell Biology
Physiology

Date 2005 Feb 11

PMID 15702480

Citations 82

Authors

Francisco J Blanco

Juan F Santibanez

Mercedes Guerrero-Esteo

Carmen Langa

Calvin P H Vary

Carmelo Bernabeu

Affiliations

Soon will be listed here.

Abstract

Transforming growth factor-beta (TGF-beta) signaling in endothelial cells is able to modulate angiogenesis and vascular remodeling, although the underlying molecular mechanisms remain poorly understood. Endoglin and ALK-1 are components of the TGF-beta receptor complex, predominantly expressed in endothelial cells, and mutations in either endoglin or ALK-1 genes are responsible for the vascular dysplasia known as hereditary hemorrhagic telangiectasia. Here we find that the extracellular and cytoplasmic domains of the auxiliary TGF-beta receptor endoglin interact with ALK-1 (a type I TGF-beta receptor). In addition, endoglin potentiates TGF-beta/ALK1 signaling, with the extracellular domain of endoglin contributing to this functional cooperation between endoglin and ALK-1. By contrast, endoglin appears to interfere with TGF-beta/ALK-5 signaling. These results suggest that the functional association of endoglin with ALK-1 is critical for the endothelial responses to TGF-beta.

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