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Titolo:
Cytochrome c mediates apoptosis in hypertensive nephrosclerosis in Dahl/Rapp rats
Autore:
Ying, WZ; Sanders, PW;
Indirizzi:
Univ Alabama, Dept Med, Div Nephrol, Ctr Nephrol Res & Training, Birmingham, AL 35294 USA Univ Alabama Birmingham AL USA 35294 & Training, Birmingham, AL 35294 USA Univ Alabama, Dept Med, Div Nephrol, Ctr Comprehens Canc, Birmingham, AL 35294 USA Univ Alabama Birmingham AL USA 35294 ehens Canc, Birmingham, AL 35294 USA Univ Alabama, Dept Med, Div Nephrol, Cell Adhes & Matrix Res Ctr, Birmingham, AL 35294 USA Univ Alabama Birmingham AL USA 35294 ix Res Ctr, Birmingham, AL 35294 USA Univ Alabama, Dept Physiol & Biophys, Birmingham, AL 35294 USA Univ Alabama Birmingham AL USA 35294 & Biophys, Birmingham, AL 35294 USA Dept Vet Affairs Med Ctr, Birmingham, AL USA Dept Vet Affairs Med Ctr Birmingham AL USA s Med Ctr, Birmingham, AL USA
Titolo Testata:
KIDNEY INTERNATIONAL
fascicolo: 2, volume: 59, anno: 2001,
pagine: 662 - 672
SICI:
0085-2538(200102)59:2<662:CCMAIH>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
SALT-RESISTANT RATS; CELL-FREE-EXTRACTS; BAX; MITOCHONDRIA; BCL-X(L); DEATH; BCL-2; POLYMERASE; ACTIVATION; INDUCTION;
Keywords:
chronic renal failure; mitochondria; caspase-9; TUNEL; end-stage renal failure; nephrosclerosis; fibrosis; programmed cell death;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Sanders, PW Univ Alabama, Dept Med, Div Nephrol, Ctr Nephrol Res & Training, 642 LyonsHarrison Res Bldg,701 19th St S, Birmingham, AL 35294 USA Univ Alabama 642 Lyons Harrison Res Bldg,701 19th St S Birmingham AL USA 35294
Citazione:
W.Z. Ying e P.W. Sanders, "Cytochrome c mediates apoptosis in hypertensive nephrosclerosis in Dahl/Rapp rats", KIDNEY INT, 59(2), 2001, pp. 662-672

Abstract

Background. Renal damage from hypertension is the second most common causeof end-stage renal failure in the United States. The pathogenesis of this process is incompletely understood. The Dahl/Rapp salt-sensitive (S) rat isa model of low-renin hypertension, but these rats also develop renal lesions that are virtually identical to human hypertensive nephrosclerosis. Methods. To explore apoptosis as a mechanism of progressive renal injury in S rats, age- and sex-matched S and Sprague-Dawley (SD) rats were placed on either 0.3 or 8.0% NaCl diets, which were continued for 21 days. Results. At day 7, renal histology appeared relatively nor mal, but by day21 on the high-salt diet, S rats displayed morphological evidence of severe renal injury that included glomerulosclerosis. arteriolosclerosis, and tubulointerstitial damage. Apoptosis was demonstrated in kidneys of hypertensive S rats by day 7. Cytoplasmic content of cytochrome c was increased in the kidney cortex of hypertensive S rats, and isolated mitochondria showed inappropriate release of cytochrome c sufficient to activate caspase-3 in vitro. Activation of caspase-9 and caspase-3 was observed only in kidney cortex from hypertensive S rats. Conclusions. Kidneys from hypertensive S rats display apoptosis related tomitochondrial release of cytochrome c and activation of caspase-9 and caspase-3. The findings support a primary role of cytochrome c release and apoptosis in the pathogenesis of hypertensive nephrosclerosis in S rats.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 13:52:16