Linked Life Data

10355733

Source:http://linkedlifedata.com/resource/pubmed/id/10355733

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-8-9
pubmed:abstractText
Compstatin, a newly described C3-binding peptide, inhibits complement activation by blocking C3 convertase-mediated cleavage of C3. As the complement activation is an essential part of the rejection reaction, we evaluated the ability of Compstatin to delay or prevent hyperacute rejection in an ex vivo xenograft model. Pig kidneys were perfused with fresh human blood containing either Compstatin (n=6) or a control agent (n=6). Graft survival and activation of complement, leukocytes and platelets both in the fluid-phase and in the tissue were examined. The survival of the Compstatin-perfused kidneys (median, 380 min) was significantly (P=0.0036) longer than that of the controls (median, 90 min). The classical complement pathway (C1rs-C1inhibitor and C4bc) was significantly and equally activated in both groups during the first 60 min. C3 activation products increased fivefold and terminal complement complex eightfold in the control group, but no increase occurred in the Compstatin group during this period. Immunohistochemistry showed less C3 and fibrin deposition and immune electron microscopy showed less terminal SC5b-9 complement complex deposition in the Compstatin group. A significant change in total white cells, neutrophils, myeloperoxidase, and expression of the surface activation markers CD11b (CR3) and CD35 (CR1) and CD62L (L-selectin) was observed in both groups. Leukocyte activation was lower in the Compstatin group but the difference was not statistically significant. There were no differences in platelet counts, thrombospondin, soluble P-selectin or beta-thromboglobulin between the groups. We conclude that Compstatin prolongs graft survival and suggest that it may be a useful agent for attenuating hyperacute rejection by inhibiting C3 and thus terminal complement pathway activation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0908-665X
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
52-65
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10355733-Animals, pubmed-meshheading:10355733-Blood Platelets, pubmed-meshheading:10355733-Complement C3b, pubmed-meshheading:10355733-Complement C3c, pubmed-meshheading:10355733-Complement Inactivator Proteins, pubmed-meshheading:10355733-Complement Membrane Attack Complex, pubmed-meshheading:10355733-Female, pubmed-meshheading:10355733-Graft Rejection, pubmed-meshheading:10355733-Graft Survival, pubmed-meshheading:10355733-Humans, pubmed-meshheading:10355733-Immunohistochemistry, pubmed-meshheading:10355733-Kidney Transplantation, pubmed-meshheading:10355733-Leukocytes, pubmed-meshheading:10355733-Male, pubmed-meshheading:10355733-Microscopy, Immunoelectron, pubmed-meshheading:10355733-Models, Biological, pubmed-meshheading:10355733-Peptides, Cyclic, pubmed-meshheading:10355733-Perfusion, pubmed-meshheading:10355733-Transplantation, Heterologous
pubmed:year
1999
pubmed:articleTitle
Compstatin, a peptide inhibitor of C3, prolongs survival of ex vivo perfused pig xenografts.
pubmed:affiliation
Department of Surgery A, University of Oslo, The National Hospital, Norway.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't