| Intrinsic resistance of hepatocytes to complement-mediated injury. | |
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MedLine Citation:
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PMID: 15905577 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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When activated on or in the vicinity of cells, complement usually causes loss of function and sometimes cell death. Yet the liver, which produces large amounts of complement proteins, clears activators of complement and activated complexes from portal blood without obvious injury or impaired function. We asked whether and to what extent hepatocytes resist injury and loss of function mediated by exposure to complement. Using cells isolated from porcine livers as a model system, we found that, in contrast to endothelial cells, hepatocytes profoundly resist complement-mediated lysis and exhibit normal synthetic and conjugative functions when complement is activated on their surface. The resistance of hepatocytes to complement-mediated injury was not a function of cell surface control of the complement cascade but rather an intrinsic resistance of the cells dependent on the PI3K/Akt pathway. The resistance of hepatocytes to complement might be exploited in developing approaches to the treatment of hepatic failure or more broadly to the treatment of complement-mediated disease. |
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Authors:
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Cody A Koch; Akiyoshi Kanazawa; Ryuta Nishitai; Bruce E Knudsen; Kiyoshi Ogata; Timothy B Plummer; Kim Butters; Jeffrey L Platt |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 174 ISSN: 0022-1767 ISO Abbreviation: J. Immunol. Publication Date: 2005 Jun |
Date Detail:
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Created Date: 2005-05-20 Completed Date: 2005-08-08 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 7302-9 Citation Subset: AIM; IM |
Affiliation:
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Transplantation Biology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antibodies, Heterophile / metabolism Binding Sites, Antibody Cells, Cultured Complement Activation / immunology Complement Inactivator Proteins / physiology* Complement System Proteins / metabolism, toxicity* Cytotoxicity, Immunologic / immunology* Endothelium, Vascular / immunology, metabolism, pathology Hepatocytes / immunology*, metabolism, pathology* Humans Immunity, Innate Immunoglobulin G / metabolism Immunoglobulin M / metabolism Signal Transduction / immunology Swine |
| Grant Support | |
ID/Acronym/Agency:
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AI049742/AI/NIAID NIH HHS; HL52297/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antibodies, Heterophile; 0/Binding Sites, Antibody; 0/Complement Inactivator Proteins; 0/Immunoglobulin G; 0/Immunoglobulin M; 9007-36-7/Complement System Proteins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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