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Titolo:
REOXYGENATION OF HYPOXIC HUMAN UMBILICAL VEIN ENDOTHELIAL-CELLS ACTIVATES THE CLASSIC COMPLEMENT PATHWAY
Autore:
COLLARD CD; VAKEVA A; BUKUSOGLU C; ZUND G; SPERATI CJ; COLGAN SP; STAHL GL;
Indirizzi:
HARVARD UNIV,SCH MED,BRIGHAM & WOMENS HOSP,DEPT ANESTHESIA BOSTON MA 02115 HARVARD UNIV,SCH MED,BRIGHAM & WOMENS HOSP,DEPT ANESTHESIA BOSTON MA 02115
Titolo Testata:
Circulation
fascicolo: 1, volume: 96, anno: 1997,
pagine: 326 - 333
SICI:
0009-7322(1997)96:1<326:ROHHUV>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
CORONARY-ARTERY OCCLUSION; MYOCARDIAL-INFARCTION; NEUTROPHIL ADHESION; MEMBRANE-PROTEINS; ISCHEMIC-INJURY; P-SELECTIN; REPERFUSION; EXPRESSION; INHIBITOR; NECROSIS;
Keywords:
ENDOTHELIUM; HYPOXIA; ISCHEMIA; REPERFUSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
C.D. Collard et al., "REOXYGENATION OF HYPOXIC HUMAN UMBILICAL VEIN ENDOTHELIAL-CELLS ACTIVATES THE CLASSIC COMPLEMENT PATHWAY", Circulation, 96(1), 1997, pp. 326-333

Abstract

Background Ischemia-reperfusion injury leads to the activation and endothelial deposition of complement. We investigated whether exposure of human umbilical vein endothelial cells (HUVECs) to hypoxia and/or reoxygenation activates complement and decrease HUVEC-surface expressionof the C3 regulatory proteins CD-46 and CD55. Methods and Results HUVECs were subjected to 0, 12, or 24 hours of hypoxia (O-2=1%) and then reoxygenated for 3 hours (O-2=21%) in the presence of 30% human serum. C3 deposition and HUVEC-surface expression of CD46 and CD55 were evaluated by ELISA and flow cytometry. C3 deposition on HUVECs subjected to 12 or 24 hours of hypoxia followed by 3 hours of reoxygenation was significantly greater than normoxic HUVECs. Inhibition of the classic but not the alternative complement pathway during reoxygenation attenuated C3 deposition. Western blot analysis of HUVEC lysates under reducing conditions demonstrated significantly increased iC3b deposition in hypoxic/reoxygenated HUVECs compared with normoxic HUVECs. FACS analysis confirmed iC3b deposition. HUVEC-surface expression of CD46 and CD55 increased after hypoxia and/or reoxygenation. Conclusions We conclude that (1) hypoxia and reoxygenation of HUVECs significantly increasesiC3b deposition on HUVECs, (2) C3 deposition after hypoxia and reoxygenation is largely mediated by the classic complement pathway, and (3)HUVEC-surface expression of CD46 and CD55 increases after hypoxia andreoxygenation. These data demonstrates that hypoxia nad reoxygenationof human endothelial cells activates the classic complement pathway despite an increase in complement C3 regulatory proteins.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 07:13:13