The N-acetylcysteine sensitive TGF-β receptor endoglin shows a defined expression pattern in liver cells

Introduction TGF-β effects are mediated by a heteroologomeric set of high affinity membrane receptors which govern upon activation central functions of hepatic stellate cells (HSC) in the course of liver fibrogenesis [1]. In a previous study we could identify the type III receptor endoglin to be expressed in HSC and myofibroblasts (MFB) [2]. Due to its functional structure, a disulfide linked homodimer, the receptor is prone to be affected by reducing substances like N-acetylcysteine (NAC), which might at least in part account for the inhibitory effect of NAC on TGF-β signaling [3]. Because of the restricted expression pattern of endoglin the NAC effect is focused on a subpopulation of liver cells excluding the most prominent liver cell type, the hepatocytes, which do not express endoglin.