Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Hypoxia-induced expression of complement receptor type 1 (CR1, CD35) in human vascular endothelial cells
Autore:
Collard, CD; Bukusoglu, C; Agah, A; Colgan, SP; Reenstra, WR; Morgan, BP; Stahl, GL;
Indirizzi:
Harvardapeut, Sch Med, Brigham & Womens Hosp, Dept Anesthesia,Ctr Expt Ther Harvard Univ Boston MA USA 02115 mens Hosp, Dept Anesthesia,Ctr Expt Ther Boston Univ, Sch Med, Dept Dermatol, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 Med, Dept Dermatol, Boston, MA 02118 USA Univ Wales Coll Med, Dept Biochem Med, Cardiff CF4 4XN, S Glam, Wales UnivWales Coll Med Cardiff S Glam Wales CF4 4XN f CF4 4XN, S Glam, Wales
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
fascicolo: 2, volume: 45, anno: 1999,
pagine: C450 - C458
SICI:
0363-6143(199902)45:2<C450:HEOCRT>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
REPERFUSION INJURY; C3B/C4B RECEPTOR; CR-1; ACTIVATION; GENE; INFLAMMATION; INDUCTION; PROTEIN; REGION; SYSTEM;
Keywords:
cytokines; tumor necrosis factor; human umbilical vein endothelial cells; C3b; cofactor activity; immune complex;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Stahl, GL Harvardapeut, Sch Med, Brigham & Womens Hosp, Dept Anesthesia,Ctr Expt Ther Harvard Univ 75 Francis St Boston MA USA 02115 sia,Ctr Expt Ther
Citazione:
C.D. Collard et al., "Hypoxia-induced expression of complement receptor type 1 (CR1, CD35) in human vascular endothelial cells", AM J P-CELL, 45(2), 1999, pp. C450-C458

Abstract

Reoxygenation of hypoxic human umbilical vein endothelial cells (HUVECs) increases protein expression of the complement regulators CD46 and CD55. As the receptor for C3b is known to be present on injured bovine endothelial cells, we investigated whether hypoxia or inflammatory mediators induce complement receptor type 1 (CR1; CD35) expression on HUVECs. CR1 protein expression increased 3.7 +/- 0.6-fold as measured by ELISA on HUVECs following hypoxia (48 h, 1% O-2) Colocalization of CD35 and von Willebrand factor by confocal microscopy confirmed that CD35 was predominantly intracellular. Lipopolysaccharide or tumor necrosis factor-alpha also significantly increased HUVEC CR1 protein expression. Western blot analysis of neutrophil or hypoxic HUVEC lysates revealed a 221-kDa CR1 band under nonreducing conditions. RT-PCR of hypoxic HUVEC mRNA revealed a single band that, after sequencing, was identified as CD35. In situ hybridization of hypoxic HUVECs, but not normoxic HUVECs or fibroblasts, demonstrated increased CD35 mRNA. Hypoxic HUVECs bound immune complexes and acted as a cofactor for factor I-mediated cleavage of C3b. Thus hypoxia induces functional HUVEC CR1 expression.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 13:02:35