Attenuation of skeletal muscle reperfusion injury with intravenous 12 amino acid peptides that bind to pathogenic IgM.
Identifieur interne : 002D78 ( Main/Merge ); précédent : 002D77; suivant : 002D79Attenuation of skeletal muscle reperfusion injury with intravenous 12 amino acid peptides that bind to pathogenic IgM.
Auteurs : Rodney K. Chan [États-Unis] ; Nicola Verna ; Jalil Afnan ; Ming Zhang ; Shahrul Ibrahim ; Michael C. Carroll ; Francis D. MooreSource :
- Surgery [ 0039-6060 ] ; 2006.
Descripteurs français
- KwdFr :
- Animaux, Banque de peptides, Immunoglobuline M (génétique), Immunoglobuline M (métabolisme), Lésion d'ischémie-reperfusion, Muscles squelettiques (anatomopathologie), Muscles squelettiques (immunologie), Peptides, Perfusions veineuses, Souris, Souris knockout, Électrophorèse sur gel de polyacrylamide.
- MESH :
- anatomopathologie : Muscles squelettiques.
- génétique : Immunoglobuline M.
- immunologie : Muscles squelettiques.
- métabolisme : Immunoglobuline M.
- Animaux, Banque de peptides, Lésion d'ischémie-reperfusion, Peptides, Perfusions veineuses, Souris, Souris knockout, Électrophorèse sur gel de polyacrylamide.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Immunoglobulin M.
- chemical , metabolism : Immunoglobulin M.
- immunology : Muscle, Skeletal.
- pathology : Muscle, Skeletal.
- Animals, Electrophoresis, Polyacrylamide Gel, Infusions, Intravenous, Mice, Mice, Knockout, Peptide Library, Peptides, Reperfusion Injury.
Abstract
The injury sustained by reperfused skeletal muscle is inflammatory and is initiated by binding of pre-formed IgM to involved tissue, followed by local complement activation and further inflammation. A clone of natural IgM has been described that initiates this injury, suggesting that specific antigens are exposed on ischemic tissues that act as ligands for this pathogenic antibody. In these experiments, we examine the properties of short peptide sequences, and their homologues, that bind to the antigen-combining site of this pathogenic IgM clone.
DOI: 10.1016/j.surg.2005.05.028
PubMed: 16455333
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pubmed:16455333Le document en format XML
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<author><name sortKey="Zhang, Ming" sort="Zhang, Ming" uniqKey="Zhang M" first="Ming" last="Zhang">Ming Zhang</name>
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<author><name sortKey="Ibrahim, Shahrul" sort="Ibrahim, Shahrul" uniqKey="Ibrahim S" first="Shahrul" last="Ibrahim">Shahrul Ibrahim</name>
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<term>Infusions, Intravenous</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>Muscle, Skeletal (immunology)</term>
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<term>Souris knockout</term>
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<front><div type="abstract" xml:lang="en">The injury sustained by reperfused skeletal muscle is inflammatory and is initiated by binding of pre-formed IgM to involved tissue, followed by local complement activation and further inflammation. A clone of natural IgM has been described that initiates this injury, suggesting that specific antigens are exposed on ischemic tissues that act as ligands for this pathogenic antibody. In these experiments, we examine the properties of short peptide sequences, and their homologues, that bind to the antigen-combining site of this pathogenic IgM clone.</div>
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