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Ascites from Patients with Encapsulating Peritoneal Sclerosis Augments NIH/3T3 Fibroblast Proliferation
Author(s) -
Masunaga Yoshinori,
Muto Shigeaki,
Asakura Shinji,
Akimoto Tetsu,
Homma Sumiko,
Kusano Eiji,
Asano Yasushi
Publication year - 2003
Publication title -
therapeutic apheresis and dialysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.415
H-Index - 53
eISSN - 1744-9987
pISSN - 1744-9979
DOI - 10.1046/j.1526-0968.2003.00087.x
Subject(s) - medicine , fibroblast , ascites , platelet derived growth factor receptor , hepatocyte growth factor , fibroblast growth factor , tyrosine kinase , cancer research , growth factor , endocrinology , biology , biochemistry , in vitro , receptor
  Encapsulating peritoneal sclerosis (EPS) remains one of the major causes of dropout in continuous ambulatory peritoneal dialysis by reducing ultrafiltration capacity. To demonstrate whether ascites from patients with EPS (EPS ascites) has fibroblast proliferation activity, we used NIH/3T3 fibroblasts to examine the effects of EPS ascites on fibroblast proliferation activity by the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay. Encapsulating peritoneal sclerosis ascites dose‐dependently augmented NIH/3T3 fibroblast proliferation. The protein kinase C inhibitors and the tyrosine kinase inhibitors partially inhibited the stimulatory effects of EPS ascites on fibroblast proliferation activity. In EPS ascites, levels of interleukin (IL)‐1β, IL‐6, IL‐8, transforming growth factor (TGF)‐β1, hepatocyte growth factor (HGF), and platelet‐derived growth factor (PDGF)‐AB were elevated. The treatment with IL‐1β, HGF, TGF‐β1, and PDGF‐AB alone or in combination at similar concentrations to those in EPS ascites exhibited small but significant fibroblast proliferation activities. We conclude that EPS ascites stimulate NIH/3T3 fibroblast proliferation via protein kinase C and tyrosine kinase. The elevated cytokine and growth factors partly contribute to the EPS ascites‐induced fibroblast proliferation.

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