Different transforming growth factor-B1 induces extracellular matrix production in rat hepatic stellate cells versus hepatic myofibroblasts, but decorin inhibits both

The main pathological feature that leads to human liver disease is the deposition and accumulation of the extracellular matrix (ECM). Different stimuli might cause liver damage, but the hepatic stellate cells (HSC) are thought to primarily produce the accumulating ECM proteins and in many pathologic conditions the transforming growth factor-B1 has a crucial role. Decorin was reported to act as a natural inhibitory agent of TGF-B1 in experimental glomerulonephritis, but there were limited data in liver disease. We measured the expression and production of a few important extracellular matrix proteins after TGFB1, Decorin stimulation and co-stimulation on HSCs and myofibroblasts (MF) in primary cell cultures. Immunocytochemistry and Western blot analysis was performed using antibodies against different types of collagens and a few other proteins and the messenger RNA expression of the same genes was also assessed. Hepatic stellate cells and myofibrobalsts demonstrated different response to TGFB1 exposure. In contrast to HSCs in which TGFB1 upregulates the different matrix protein mRNA levels and also increases the protein synthesis no significant changes could be detected in hepatic myofibroblasts. The most remarkable effect of TGFB1 treatment was observed on Collagen type I protein. Decorin itself has a limited effect on the matrix production of HSCs and MFs. However, when we applied it in combination with TGFB1 it was capable to inhibit the effect of the growth factor.