Linked Life Data

17381529

Source:http://linkedlifedata.com/resource/pubmed/id/17381529

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-3-26
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1744-9979
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
94-100
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
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.
pubmed:affiliation
Department of Molecular and Internal Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.
pubmed:publicationType
Journal Article