Linked Life Data

10082670

Source:http://linkedlifedata.com/resource/pubmed/id/10082670

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-12-17
pubmed:abstractText
Lipopolysaccharides (LPS) induces intrahepatic cholestasis and canalicular multispecific organic anion transporter (CMOAT/MRP2) plays a central role in hepatic bilirubin transport. This study examined the role of Kupffer cell in LPS-induced cholestasis. Rats were injected intravenously with LPS. Kupffer cells were inactivated with gadolinium chloride (Gd). CMOAT/MRP2 mRNA expression was time- and dose-dependently decreased by LPS injection with a decrease in bile flow and an increase in serum bilirubin level. Gd pretreatment inhibited decrease in CMOAT/MRP2 mRNA and bile flow, and increase in serum bilirubin. Kupffer cell-conditioned medium decreased CMOAT/MRP2 expression. Addition of anti-IL-1 or anti-TNFalpha antibody restored CMOAT/MRP2 expression, whereas IL-1 and TNFalpha decreased the expression. MAP kinases were activated by addition of the conditioned medium, and addition of PD98059 or SB203580 restored CMOAT/MRP2 expression. These results suggest that LPS activates Kupffer cells to secrete IL-1 and TNFalpha, which in turn activate MAP kinases and decrease CMOAT/MRP2 expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0006-291X
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Academic Press.
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
255
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
143-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Kupffer cell-mediated down regulation of rat hepatic CMOAT/MRP2 gene expression.
pubmed:affiliation
Biomedical Research Center, Osaka University Medical School, Osaka University Medical School, Yamadaoka 2-2, Suita, Osaka, 565-0871, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't