Linked Life Data

9126863

Source:http://linkedlifedata.com/resource/pubmed/id/9126863

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
17
pubmed:dateCreated
1997-5-20
pubmed:abstractText
Rat kallikrein-binding protein (RKBP) is a negative acute phase protein. The potential role of RKBP in inflammation was evaluated in transgenic mice overexpressing the RKBP gene under the control of the mouse metallothionein metal-responsive promoter. Bacterial endotoxic lipopolysaccharide (LPS) was injected intraperitoneally into mice at a dose of 600 microg/25 g body weight. The death toll was recorded every 12 hours for 3 days. The survival rate of transgenic male mice (n=78) was 33.3% while that of control male mice (n=54) was 9.3% 3 days post LPS injection. In comparison, the survival rate of transgenic female mice (n=59) was 55.9% while that of control female mice (n=65) was 30.8%. Recombinant RKBP levels in the circulation of these mice increased by 3-fold after LPS treatment. The results show that RKBP transgenic mice have a higher survival rate than their non-transgenic control littermates after endotoxin shock and female mice are more resistant to lethality induced by endotoxin shock than male mice in both transgenic and control groups. These findings suggest that kallikrein-binding protein has a protective effect during acute phase inflammation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1431-5
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Beneficial effects of kallikrein-binding protein in transgenic mice during endotoxic shock.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston 29425, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.