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Titolo:
Predominant role for C5b-9 in renal ischemia/reperfusion injury
Autore:
Zhou, WD; Farrar, CA; Abe, K; Pratt, JR; Marsh, JE; Wang, Y; Stahl, GL; Sacks, SH;
Indirizzi:
Univ London Kings Coll, Guys Hosp, Dept Nephrol & Transplantat, London SE19RT, England Univ London Kings Coll London England SE1 9RT at, London SE19RT, England Alexion Pharmaceut, New Haven, CT USA Alexion Pharmaceut New Haven CT USA lexion Pharmaceut, New Haven, CT USA Harvard Univ, Sch Med, Ctr Expt Therapeut & Reperfus Injury, Dept Anesthesia,Brigham & Womens Hosp, Boston, MA USA Harvard Univ Boston MA USA sthesia,Brigham & Womens Hosp, Boston, MA USA
Titolo Testata:
JOURNAL OF CLINICAL INVESTIGATION
fascicolo: 10, volume: 105, anno: 2000,
pagine: 1363 - 1371
SICI:
0021-9738(200005)105:10<1363:PRFCIR>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISCHEMIA-REPERFUSION INJURY; TUBULAR EPITHELIAL-CELLS; MYOCARDIAL INFARCT SIZE; POLYMORPHONUCLEAR LEUKOCYTES; PATHWAY COMPLEMENT; ENDOTHELIAL-CELLS; SKELETAL-MUSCLE; C5A RECEPTOR; NEUTROPHILS; ACTIVATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Sacks, SH Univ London Kings Coll, Guys Hosp, Dept Nephrol & Transplantat, 5th Floor,Thomas Guy House,St Thomas St, London SE1 9RT, England Univ London Kings Coll 5th Floor,Thomas Guy House,St Thomas St London England SE1 9RT
Citazione:
W.D. Zhou et al., "Predominant role for C5b-9 in renal ischemia/reperfusion injury", J CLIN INV, 105(10), 2000, pp. 1363-1371

Abstract

Previous work has indicated that complement is a mediator of ischemia/reperfusion (I/R) injury. To investigate the components of complement responsible for this effect, we examined a model of renal I/R injury in C3-, C4-, C5-, and CG-deficient mice. We occluded the renal arteries and veins (40-58 minutes) and, after reperfusion (0-72 hours), assessed renal structural and functional injury. C3-, C5-, and C6-deficient mice were protected from renal I/R injury, whereas C4-deficient mice were not protected. C6-deficient mice treated with antibody to block C5a generation showed no additional protection from I/R injury. Reconstitution with C6 alone restored the I/R injuryin CG-deficient mice. Tubular epithelial cells were the main structures damaged by complement-mediated attack, and, in contrast, the renal vessels were spared. Neutrophil infiltration and myeloperoxidase activity were reduced in C-deficient mouse kidney but by a similar extent in C3-deficient and CG-deficient mice. We conclude that the membrane attack complex of complement tin which C5 and CG participate) may account for the effect of complementon mouse renal I/R injury. Neither C5a-mediated neutrophil infiltration nor the classic pathway in which C4 participates, appears to contribute to I/R injury in this model. By contrast with other organs, such as the heart, the primary effect of complement in the ischemic area is on the parenchymal cell rather than the vascular endothelial cell. The membrane attack complexof complement is a Potential target for prevention of I/R injury in this model.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/04/20 alle ore 04:11:31