Koki Matsuo a , Yasuhiro Maeda a , Yoshito Naiki a , Toshiaki Matsuoka a , Yoshihisa Tamai a , Satoru Yonekawa a , Mika Sakaguchi a , Ichiro Iwamoto a , Hirohumi Hasegawa a , Kunio Matsumoto b , Toshikazu Nakamura b , Akihisa Kanamaru a
20 January 2005
Objective: Some patients who had carried out long-term continuous ambulatory peritoneal dialysis discontinued the treatment because of progressive peritoneal fibrosis. It has been previously reported that transforming growth factor-β<sub>1</sub> (TGF-β<sub>1</sub>) is one of the factors that induces peritoneal fibrosis. Also, hepatocyte growth factor (HGF) plays a role in the prevention of fibrosis and in inhibiting TGF-β<sub>1</sub> production. In this study, we examined the effects of HGF on peritoneal fibrosis by TGF-β<sub>1</sub> induced by high concentrations of D-glucose. Design: We transfected a full-length human HGF cDNA in an expression vector into human peritoneal mesothelial cells (HPMCs) using the calcium phosphate method. Transfected HPMCs were cultured with high concentrations of D-glucose solution and co-cultured with fibroblasts using a transwell system. Cell proliferation was determined using the Tetra Color One method. TGF-β<sub>1</sub> and HGF protein were measured by enzyme-linked immunosorbent assay. Results: In addition to recombinant HGF, the growth inhibition of HPMCs by high concentration D-glucose or TGF-β<sub>1</sub> was significant. By transfecting HGF cDNA into HPMCs, growth inhibition by high concentration D-glucose was completely restored. Furthermore, the production of TGF-β<sub>1</sub> was also significantly decreased. Conclusion: These results suggested that exogenous HGF could possibly prevent peritoneal fibrosis.