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Titolo:
Endothelial nuclear factor-kappa B translocation and vascular cell adhesion molecule-1 induction by complement inhibition with anti-human C5 therapy or cGMP analogues
Autore:
Collard, CD; Agah, A; Reenstra, W; Buras, J; Stahl, GL;
Indirizzi:
Harvard Univ, Brigham & Womens Hosp, Ctr Expt Therapeut & Reperfus Injury,Sch Med,Dept Anesthesia, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 ed,Dept Anesthesia, Boston, MA 02115 USA Harvard Univ, Brigham & Womens Hosp, Ctr Expt Therapeut & Reperfus Injury,Sch Med,Dept Clin Pathol, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 d,Dept Clin Pathol, Boston, MA 02115 USA Harvard Univ, Brigham & Womens Hosp, Ctr Expt Therapeut & Reperfus Injury,Sch Med,Dept Emergency Med, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 Dept Emergency Med, Boston, MA 02115 USA
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 11, volume: 19, anno: 1999,
pagine: 2623 - 2629
SICI:
1079-5642(199911)19:11<2623:ENFBTA>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
MEMBRANE ATTACK COMPLEX; MONOCYTE CHEMOATTRACTANT PROTEIN-1; NITRIC-OXIDE; P-SELECTIN; REPERFUSION INJURY; MICROVASCULAR ENDOTHELIUM; CARDIOPULMONARY BYPASS; ATHEROSCLEROTIC LESION; ISCHEMIA-REPERFUSION; IN-VIVO;
Keywords:
adhesion molecules; hypoxia; inflammation; nitric oxide; immunotherapy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Stahl, GL Harvard Univ, Brigham & Womens Hosp, Ctr Expt Therapeut & Reperfus Injury,Sch Med,Dept Anesthesia, Boston, MA 02115 USA Harvard Univ Boston MA USA 02115 esthesia, Boston, MA 02115 USA
Citazione:
C.D. Collard et al., "Endothelial nuclear factor-kappa B translocation and vascular cell adhesion molecule-1 induction by complement inhibition with anti-human C5 therapy or cGMP analogues", ART THROM V, 19(11), 1999, pp. 2623-2629

Abstract

We have previously shown that reoxygenation of hypoxic human umbilical vein endothelial cells (HUVECs) leads to the activation and deposition of complement. In the present study, we investigated whether the terminal complement complex (C5b-9) influences HUVEC nuclear factor-kappa B (NF-kappa B) translocation and vascular cell adhesion molecule-1 (VCAM-1) protein expression after hypoxia/reoxygenation by decreasing endothelial cGMP. Additionally,we investigated the action of anti-human C5 therapy on endothelial cGMP, NF-kappa B translocation, and VCAM-1 protein expression. Reoxygenation (0.5 to 3 hours, 21% O-2) of hypoxic (12 hours, 1% O-2) HUVECs in human serum (HS) significantly increased C5b-9 deposition, VCAM-1 expression, and NF-kappa B translocation compared with hypoxic/reoxygenated HUVECs treated with the recombinant human C5 inhibitor h5G1.1scFv. Acetylcholine (ACh)-induced cGMP synthesis was significantly higher in normoxic HUVECs compared with hypoxic HUVECs reoxygenated in HS but did not differ from hypoxic HUVECs reoxygenated in buffer or HS treated with h5G1.1-scFv. Treatment of hypoxic/reoxygenated HUVECs with h5G1.1-scFv or cGMP analogues significantly attenuated NF-kappa B translocation and VCAM-1 protein expression, Treatment with NO analogues, but not a cAMP analogue, cGMP antagonists, or an NO antagonist, also significantly attenuated VCAM-1 expression. We conclude that (1) C5b-9 deposition, NF-kappa B translocation, and VCAM-1 protein expression are increased in hypoxic HUVECs reoxygenated in HS; (2) reoxygenation of hypoxic HUVECs in HS, but not buffer alone, attenuates ACh-induced cGMP synthesis; and (3) treatment of hypoxic/reoxygenated HUVECs with h5G1.1-scFv attenuatesC5b-9 deposition, NF-kappa B translocation, and VCAM-1 expression while preserving ACh-induced cGMP synthesis, C5b-9-induced VCAM-1 expression may thus involve an NO/cGMP-regulated NF-kappa B translocation mechanism.

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Documento generato il 05/04/20 alle ore 03:15:04