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

Introduction: TGF-β is the major cytokine regulating hepatic stellate cell (HSC) function in the course of liver fibrogenesis [1]. In a previous study we demonstrated that the reducing substance N-Acetylcysteine (NAC) is able to block TGF-β signaling in HSC by different means than modification of the cellular redox state. As one target we could identify the type III receptor, endoglin, which is 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, and is therefore monomerized in our experimental setting. 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.