Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
|
pubmed:dateCreated |
1990-11-2
|
pubmed:abstractText |
We have studied the secretion of proteins of the alternative pathway of complement C3, factor B and factor H by human umbilical vein endothelial cells (HUVEC). Results showed that factor H and factor B are quantitatively secreted in abundance whereas C3 could only be detected when the cells are maintained in culture during long periods of time. Interferon-gamma stimulated factor H, factor B and, to a lesser extent, C3 secretions. Interleukin (IL) 1 had a differential effect on spontaneous C3, factor B and factor H secretions. In the presence of IL 1, there was a significant secretion of C3 occurring within a short period of culture. IL 1 also stimulated factor B secretion. There was a synergistic stimulating effect between IL 1 and interferon-gamma to bring C3 and factor B productions by HUVEC to very high levels. In contrast, factor H secretion was consistently inhibited by IL 1. Local increase in C3 and factor B secretions by endothelial cells in the presence of IL 1 may have important implications in the inflammatory reaction. In striking contrast, the glucocorticoid dexamethasone (DXM) had modulatory effects which are consistent with its anti-inflammatory properties. DXM, at therapeutic concentrations, decreased C3 and factor B secretions and increased factor H secretion. Local modulation of complement protein secretion by DXM appears to be a new mechanism by which this glucocorticoid may control inflammation.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Complement C3b Inactivator Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C3c,
http://linkedlifedata.com/resource/pubmed/chemical/Complement Factor B,
http://linkedlifedata.com/resource/pubmed/chemical/Complement Factor H,
http://linkedlifedata.com/resource/pubmed/chemical/Complement Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Dexamethasone,
http://linkedlifedata.com/resource/pubmed/chemical/Glucocorticoids,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Serine Endopeptidases,
http://linkedlifedata.com/resource/pubmed/chemical/complement factor H, human
|
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
0014-2980
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
20
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1669-75
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:2145163-Complement C3b Inactivator Proteins,
pubmed-meshheading:2145163-Complement C3c,
pubmed-meshheading:2145163-Complement Factor B,
pubmed-meshheading:2145163-Complement Factor H,
pubmed-meshheading:2145163-Complement Factor I,
pubmed-meshheading:2145163-Complement Pathway, Alternative,
pubmed-meshheading:2145163-Dexamethasone,
pubmed-meshheading:2145163-Endothelium,
pubmed-meshheading:2145163-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:2145163-Gene Expression Regulation,
pubmed-meshheading:2145163-Glucocorticoids,
pubmed-meshheading:2145163-Humans,
pubmed-meshheading:2145163-Interleukin-1,
pubmed-meshheading:2145163-Serine Endopeptidases
|
pubmed:year |
1990
|
pubmed:articleTitle |
Expression of complement alternative pathway proteins by endothelial cells. Differential regulation by interleukin 1 and glucocorticoids.
|
pubmed:affiliation |
INSERM U-78, Bois-Guillaume, France.
|
pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
|