Linked Life Data

11367531

Source:http://linkedlifedata.com/resource/pubmed/id/11367531

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-5-22
pubmed:abstractText
Growing evidence obtained in recent years indicates that anaphylatoxin C5a receptors (C5aR) are not restricted to myeloid cells but are also expressed on nonmyeloid cells in different tissues such as brain, lung, skin and liver. In contrast to its well-defined systemic functions, the actions of anaphylatoxins in these organs are poorly characterized. The liver can be a primary target organ for the C5a anaphylatoxin since the liver is directly connected to the gut, via the mesenteric veins and portal vein which is a main source of complement activating lipopolysaccharides (LPS). In the normal rat liver, the C5aR is only expressed by nonparenchymal cells, i.e. strongly by Kupffer cells (KC) and hepatic stellate cells (HSC) and weakly by sinusoidal endothelial cells (SEC), but not expressed by the parenchymal hepatocytes (HC). Accordingly, direct effects of C5a were only found in the C5aR-expressing KC and HSC: C5a induced the release of prostanoids from KC and HSC and enhanced the LPS-dependent release of interleukin-6 from KC. These soluble mediators indirectly influenced effector functions of the C5aR-free HC. C5a enhanced the glycogen phosphorylase activity and thus the glucose output from HC indirectly via prostanoids released from KC and HSC. Glucose can serve as an energy substrate as well as an electron donor for the synthesis of reactive oxygen intermediates by KC. Moreover, C5a also enhanced transcription of the gene for the type-2 acute phase protein alpha 2-macroglobulin in HC indirectly by increasing LPS-dependent IL-6 release from KC. Under pathological conditions, C5aR was found to be upregulated in various organs including the liver. Simulation of inflammatory conditions by treatment of rats with IL-6, a main inflammatory mediator in the liver, caused a de novo expression of functional C5aR in HC. In livers of IL-6-treated rats, C5a initiated glucose output from HC and perhaps other HC-specific defense reactions directly without the intervention of soluble mediators from nonparenchymal cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1567-5769
pubmed:author
pubmed:issnType
Print
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
469-81
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Functions of anaphylatoxin C5a in rat liver: direct and indirect actions on nonparenchymal and parenchymal cells.
pubmed:affiliation
Institut für Biochemie und Molekulare Zellbiologie, Georg-August-Universität Göttingen, Humboldtallee 23, D-37073 Göttingen, Germany. hschief@gwdg.de
pubmed:publicationType
Journal Article, In Vitro, Review