6533b85ffe1ef96bd12c26b6
RESEARCH PRODUCT
C7 is expressed on endothelial cells as a trap for the assembling terminal complement complex and may exert anti-inflammatory function.
Paola PicottiPaola PicottiRoberta BullaClaudio TripodoFleur BossiReinhard WürznerElena BettoCarlo PucilloPaolo MacorLucia RizziAlessandra DebeusFrancesco Tedescosubject
ProteomicsVasculitisUmbilical VeinsVasculitiImmunologyComplementComplement; C7; endothelial cells; inflammationComplement Membrane Attack ComplexBiologyBiochemistryProinflammatory cytokineWestern blotmedicineHumansVimentinC7Interleukin 8Northern blotRNA MessengerMembrane ProteinCells CulturedGel electrophoresisEndothelial Cellmedicine.diagnostic_testCell adhesion moleculeComplement; endothelial cells; inflammationInterleukin-8Endothelial CellsMembrane ProteinsProteomicUmbilical VeinHematologyCell BiologyMolecular biologyComplement C7Endothelial stem cellCells Cultured; Complement C7; Complement Membrane Attack Complex; Endothelial Cells; Humans; Interleukin-8; Membrane Proteins; Proteomics; RNA Messenger; Umbilical Veins; Vasculitis; Vimentin; Hematology; Biochemistry; Cell Biology; Immunologyinflammationendothelial cellComplement membrane attack complexHumandescription
AbstractWe describe a novel localization of C7 as a membrane-bound molecule on endothelial cells (ECs). Data obtained by sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE), Western blot analysis, Northern blot analysis, and mass spectrometry revealed that membrane-associated C7 (mC7) was indistinguishable from soluble C7 and was associated with vimentin on the cell surface. mC7 interacted with the other late complement components to form membrane-bound TCC (mTCC). Unlike the soluble SC5b-9, mTCC failed to stimulate ECs to express adhesion molecules, to secrete IL-8, and to induce albumin leakage through a monolayer of ECs, and more importantly protected ECs from the proinflammatory effect of SC5b-9. Our data disclose the possibility of a novel role of mC7 that acts as a trap for the late complement components to control excessive inflammation induced by SC5b-9.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2009-01-01 |