<Originals>Possible involvement of the TGF-β1 signal in the development of peritoneal sclerosis as one of the major complications in continuous ambulatory peritoneal dialysis

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Background. In long term continuous ambulatory peritoneal dialysis (CAPD), the functional failure of the peritoneal membrane is the most serious problem. Transforming growth factor-beta (TGF-β) is one of the key mediators of fibrosis in some organs, and it was suggested to participate in the alteration of peritoneal function. In this study, the role of TGF-β1/TGF-β receptors for the proliferation of human peritoneal mesothelial cells (HPMCs) and fibroblasts and their interactions in CAPD patients were examined. Methods and Results. HPMCs were cultured for 48 hr in a medium containing normal dose glucose (7 mM), high dose glucose (30 mM) and mannitol as an osmotic agent equal to that of 30 mM glucose. Cell proliferation was observed using Tetra Color One assay. The concentration of TGF-β1 in culture supernatants was measured by enzyme-linked immunosorbent assay (ELISA). The expressions of TGF-β receptor types I and II were observed by flow cytometry. Co-culture assay of HPMCs and fibroblasts using transwell inserts was performed to identify the effects of the high concentration glucose solution. The proliferation of HPMCs was inhibited by a high concentration of glucose but not by that of mannitol. The inhibition was restored by the neutralizing antibody for TGF-β1. The concentration of TGF-β1 was induced by a high concentration of glucose but not by a high concentration of mannitol as an osmotic agent. Furthermore, the expressions of both TGF-β receptors were augmented by being cultured with a high concentration of glucose but not by mannitol. In the co-culture assay, the cell number of HPMCs was decreased and the cell number of fibroblasts was increased significantly by culturing with a high concentration of glucose in the same dimension. Conclusion. A high concentration of glucose induced a large quantity of TGF-β1 and enhanced the expression of TGF-β receptors. This study demonstrated that HPMCs were sensitive to TGF-β1 in response to a high concentration of glucose. These findings suggested that TGF-β1 from HPMCs exposed to a high concentration of glucose suppresses the proliferation of HPMCs and accelerates peritoneal fibrosis.
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<Originals>Possible involvement of the TGF-β1 signal in the development of peritoneal sclerosis as one of the major complications in continuous ambulatory peritoneal dialysis

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