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Titolo:
The von Hippel-Lindau gene product inhibits renal cell apoptosis via Bcl-2-dependent pathways
Autore:
Devarajan, P; De Leon, M; Talasazan, F; Schoenfeld, AR; Davidowitz, EJ; Burk, RD;
Indirizzi:
Albert Einstein Coll Med, Dept Pediat, Div Pediat Nephrol, Bronx, NY 10461USA Albert Einstein Coll Med Bronx NY USA 10461 t Nephrol, Bronx, NY 10461USA Albert Einstein Coll Med, Dept Microbiol & Immunol, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 Immunol, Bronx, NY 10461 USA Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10461 USA Albert EinsteinColl Med Bronx NY USA 10461 t Pediat, Bronx, NY 10461 USA Albert Einstein Coll Med, Dept Epidemiol & Social Med, Bronx, NY 10461 USAAlbert Einstein Coll Med Bronx NY USA 10461 cial Med, Bronx, NY 10461 USA Albert Einstein Coll Med, Marion Bessin Liver Res Ctr, Bronx, NY 10461 USAAlbert Einstein Coll Med Bronx NY USA 10461 Res Ctr, Bronx, NY 10461 USA Albert Einstein Coll Med, Albert Einstein Comprehens Canc Ctr, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 Canc Ctr, Bronx, NY 10461 USA
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 44, volume: 276, anno: 2001,
pagine: 40599 - 40605
SICI:
0021-9258(20011102)276:44<40599:TVHGPI>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-SUPPRESSOR GENE; BCL-2 FAMILY MEMBERS; ATP DEPLETION; CYTOCHROME-C; MEDIATED APOPTOSIS; UBIQUITIN LIGASE; CARCINOMA-CELLS; PROTEIN; INJURY; DEATH;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Devarajan, P Ctr Childrens Kidney, 3326 Bainbridge Ave, Bronx, NY 10467 USA Ctr Childrens Kidney 3326 Bainbridge Ave Bronx NY USA 10467 A
Citazione:
P. Devarajan et al., "The von Hippel-Lindau gene product inhibits renal cell apoptosis via Bcl-2-dependent pathways", J BIOL CHEM, 276(44), 2001, pp. 40599-40605

Abstract

Previous studies have reported a protective role for the von Hippel-Lindau(VHL) gene products against proapoptotic cellular stresses, but the mechanisms remain unclear. In this study, we examined the role of VHL in renal cells subjected to chemical hypoxia, using four VHL-negative and two VHL-positive cell lines. VHL-negative renal carcinoma cells underwent apoptosis following chemical hypoxia (short-term glucose deprivation and antimycin treatment), as evidenced by morphologic changes and internucleosomal DNA cleavage. Reintroduction of VHL expression prevented this apoptosis. VHL-negative cells displayed a significant (greater than 5-fold) activation of caspase 9and release of cytochrome c into the cytosol following chemical hypoxia. In contrast, VHL-positive cells showed minimal caspase 9 activation, and absence of cytochrome c release under the same conditions. Caspase 8 was only minimally activated in both VHL-negative and -positive cells. In addition, VHL-positive cells displayed a striking up-regulation of Bcl-2 expression (5-fold) following chemical hypoxia. Antisense oligonucleotides to Bcl-2 significantly down-regulated Bcl-2 protein expression in VHL-positive cells and rendered them sensitive to apoptosis. Overexpression of Bcl-2 in VHL-negative cells conferred resistance to apoptosis. Our results suggest that VHL protects renal cells from apoptosis via Bcl-2-dependent pathways.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/21 alle ore 07:45:42