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Titolo:
Endothelial expression of VCAM-1 in experimental crescentic nephritis and effect of antibodies to very late antigen-4 or VCAM-1 on glomerular injury
Autore:
Allen, AR; McHale, J; Smith, J; Cook, HT; Karkar, A; Haskard, DO; Lobb, RR; Pusey, CD;
Indirizzi:
HammersmithN,osp, Imperial Coll, Sch Med, Div Med,Renal Sect, London W12 0N Hammersmith Hosp London England W12 0NN iv Med,Renal Sect, London W12 0N HammersmithLungp, Imperial Coll, Sch Med,Cardiovasc Med Unit, Natl Heart &Hammersmith Hosp London England W12 0NN ardiovasc Med Unit, Natl Heart & Biogen Inc, Cambridge, MA 02142 USA Biogen Inc Cambridge MA USA 02142Biogen Inc, Cambridge, MA 02142 USA
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 9, volume: 162, anno: 1999,
pagine: 5519 - 5527
SICI:
0022-1767(19990501)162:9<5519:EEOVIE>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-ADHESION MOLECULE-1; IMMUNE-COMPLEX GLOMERULONEPHRITIS; ANTI-GBM GLOMERULONEPHRITIS; CD8 POSITIVE CELLS; IN-VIVO; MONOCLONAL-ANTIBODY; P-SELECTIN; WKY RATS; AUTOIMMUNE GLOMERULONEPHRITIS; LYMPHOCYTE RECIRCULATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
62
Recensione:
Indirizzi per estratti:
Indirizzo: Allen, AR Hammersmithondon, Imperial Coll, Sch Med, Div Med,Renal Sect, DuCane Rd, L Hammersmith Hosp Du Cane Rd London England W12 0NN u Cane Rd, L
Citazione:
A.R. Allen et al., "Endothelial expression of VCAM-1 in experimental crescentic nephritis and effect of antibodies to very late antigen-4 or VCAM-1 on glomerular injury", J IMMUNOL, 162(9), 1999, pp. 5519-5527

Abstract

The migration of leukocytes into glomeruli in crescentic glomerulonephritis is fundamental to pathogenesis, and offers important therapeutic opportunities. We addressed the importance of VCAM-1, and its leukocyte ligand verylate antigen-4 (VLA-4), in such leukocyte migration. In a rat model of nephrotoxic nephritis, glomerular expression of VCAM-1, studied by immunohistochemistry, was up-regulated by day 6 of nephritis, To quantify kidney endothelial VCAM-1 expression, a differential radiolabeled mAb technique was used, which demonstrated that protein expression was not up-regulated by day 2of nephritis, but rose threefold between days 2 and 5, and remained elevated until at least day 28, An in vivo study was then performed, using blocking mAbs to either VCAM-1 or VLA-4, starting mAb treatment on the day prior to disease induction, and continuing until animals were sacrificed at day 7, mAbs to VLA-4 significantly attenuated renal injury (albuminuria, glomerular fibrinoid necrosis, and crescent formation), but mAbs to VCAM-1 had no significant effect. Surprisingly, the number of leukocytes within glomeruliwas unaffected by anti-VLA-4 mAb therapy, despite the reduction in renal injury. Paradoxically, classical markers of macrophage activation were increased in the anti-VLA-4- and anti-VCAM-1-treated animals. This study demonstrates that kidney endothelial VCAM-1, in contrast to ICAM-1, is not up-regulated by day 2 of nephrotoxic nephritis, and plays little part in early leukocyte influx into glomeruli, However, VLA-4 is an important mediator of glomerular injury, operating after transendothelial leukocyte migration, and presumably binding to alternate ligands within the kidney.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 19:43:37