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

:  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...

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Published inTherapeutic apheresis and dialysis Vol. 11; no. 2; pp. 94 - 100
Main Authors Katsutani, Masahira, Ito, Takafumi, Masaki, Takao, Kohno, Nobuoki, Yorioka, Noriaki
Format Journal Article
LanguageEnglish
Published Melbourne, Australia Blackwell Publishing Asia 01.04.2007
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Summary::  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.
Bibliography:istex:572E213C5201CE85152461C8B2AC8C7C06E70662
ark:/67375/WNG-SLC26SZS-N
ArticleID:TAP423
ISSN:1744-9979
1744-9987
DOI:10.1111/j.1744-9987.2007.00423.x