Endoglin modulates Smad-dependent and Smad-independent pathways to regulate proliferation, migration and profibrogenic responses in myofibroblasts

Abstract

Aims: TGF-β1-mediated transdifferentiation of hepatic stellate cells (HSC) to myofibroblast-like cells (MFB) is the key event to initiate the fibrogenic program in the liver. This comprises upregulation of contractile elements, e.g. α-SMA, increased expression of collagen type I and connective tissue growth factor (CTGF) as well as a higher proliferation and migration rate [1]. To determine the factors that govern myoblast conversion upon TGF-β1-treatment in more detail, we analyzed a model system for TGF-β1-signaling, i.e. myoblasts, which display a myofibroblast-like phenotype when cultured in the presence of TGF-β1 [2].