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Glucose‐Based PD Solution, But Not Icodextrin‐Based PD Solution, Induces Plasminogen Activator Inhibitor‐1 and Tissue‐Type Plasminogen Activator in Human Peritoneal Mesothelial Cells via ERK1/2
Author(s) -
Katsutani Masahira,
Ito Takafumi,
Masaki Takao,
Kohno Nobuoki,
Yorioka Noriaki
Publication year - 2007
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 - 10.1111/j.1744-9987.2007.00423.x
Subject(s) - icodextrin , medicine , plasminogen activator , plasminogen activator inhibitor 1 , peritoneal dialysis , extracellular , endocrinology , pharmacology , biochemistry , chemistry
Peritoneal dialysis (PD) solutions containing glucose are considered to cause peritoneal fibrosis. Plasminogen activator inhibitor‐1 (PAI‐1) and tissue‐type plasminogen activator (t‐PA) participate in fibrogenesis of various organs, and human peritoneal mesothelial cells (HPMC) can produce PAI‐1 and t‐PA following glucose stimulation. Icodextrin has been widely used as an alternative osmotic agent. In this study, we investigated whether icodextrin‐based PD solution reduced the production of PAI‐1 and t‐PA by HPMC. We also examined the involvement of extracellular signal‐regulated kinase 1/2 (ERK1/2). Glucose‐based PD solutions increased the production of PAI‐1 and t‐PA by HPMC, whereas icodextrin‐based PD solution exerted lesser effects. Glucose‐based PD solutions activated ERK1/2, and PD98059 inhibited the production of PAI‐1 and t‐PA—responses not observed with icodextrin‐based PD solution. In conclusion, glucose ‐ based PD solutions, unlike icodextrin‐based PD solution, induce overproduction of PAI‐1 and t‐PA via the ERK1/2 pathway.