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Titolo:
CLUSTERIN DEPLETION ENHANCES IMMUNE GLOMERULAR INJURY IN THE ISOLATED-PERFUSED KIDNEY
Autore:
SAUNDERS JR; AMINIAN A; MCRAE JL; OFARRELL KA; ADAM WR; MURPHY BF;
Indirizzi:
ST VINCENTS HOSP,DEPT NEPHROL,41 VICTORIA PARADE FITZROY VIC 3065 AUSTRALIA ST VINCENTS HOSP,DEPT NEPHROL MELBOURNE VIC AUSTRALIA UNIV MELBOURNE,DEPT MED MELBOURNE VIC AUSTRALIA HEIDELBERG REPATRIAT HOSP,RENAL UNIT MELBOURNE VIC AUSTRALIA
Titolo Testata:
Kidney international
fascicolo: 3, volume: 45, anno: 1994,
pagine: 817 - 827
SICI:
0085-2538(1994)45:3<817:CDEIGI>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
MEMBRANE ATTACK COMPLEX; RETE TESTIS FLUID; SULFATED GLYCOPROTEIN-2; MONOCLONAL-ANTIBODIES; CHROMAFFIN GRANULES; GENE-EXPRESSION; MESSENGER-RNA; DEPOSITS; PROTEIN; TISSUE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
J.R. Saunders et al., "CLUSTERIN DEPLETION ENHANCES IMMUNE GLOMERULAR INJURY IN THE ISOLATED-PERFUSED KIDNEY", Kidney international, 45(3), 1994, pp. 817-827

Abstract

Clusterin is a normal plasma protein, shown to be an inhibitor of reactive complement hemolysis and a component of the fluid phase SC5b-9 terminal complement complexes. It is a component of glomerular immune deposits in human and experimental glomerulonephritis. Using the complement-dependent isolated perfused rat kidney model of autologous phase passive Heymann nephritis, we have studied the effect of clusterin depletion of perfused plasma on the development of glomerular injury. Kidneys with planted glomerular sheep anti-rat Fx1A antibody were perfused with human plasma either depleted of clusterin to less than or equalto 30%, or control plasma depleted of plasma fibronectin. Glomerular injury was then initiated by the addition of guinea pig anti-sheep immunoglobulins to the perfusate. Kidneys perfused with clusterin depleted plasma developed significantly greater proteinuria at all time points when compared to control kidneys. Glomerular antibody binding and C3deposition were similar in the two groups, but terminal complement components were deposited in larger amounts in the clusterin depleted group. These data support a possible role for clusterin in vivo in the protection of complement-induced glomerular injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 22:11:08