Coronary vessel development is dependent on the type III transforming growth factor beta receptor.

Transforming growth factor (TGF)beta receptor III (TGFbetaR3), or beta-glycan, binds all 3 TGFbeta ligands and inhibin with high affinity but lacks the serine/threonine kinase domain found in the type I and type II receptors (TGFbetaR1, TGFbetaR2). TGFbetaR3 facilitates signaling via TGFbetaR1/TGFbetaR2 but also has been suggested to play a unique and nonredundant role in TGFbeta signaling. Targeted deletion of Tgfbr3 revealed a requirement for Tgfbr3 during development of the coronary vessels.

Transforming growth factor-beta induces loss of epithelial character and smooth muscle cell differentiation in epicardial cells.

During embryogenesis, epicardial cells undergo epithelial-mesenchymal transformation (EMT), invade the myocardium, and differentiate into components of the coronary vasculature, including smooth muscle cells. We tested the hypothesis that transforming growth factor-beta (TGFbeta) stimulates EMT and smooth muscle differentiation of epicardial cells. In epicardial explants, TGFbeta1 and TGFbeta2 induce loss of epithelial morphology, cytokeratin, and membrane-associated Zonula Occludens-1 and increase the smooth muscle markers calponin and caldesmon.