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Titolo:
BCL-2 INHIBITS GLUCOCORTICOID-INDUCED APOPTOSIS BUT ONLY PARTIALLY BLOCKS CALCIUM IONOPHORE OR CYCLOHEXIMIDE-REGULATED APOPTOSIS IN S49 CELLS
Autore:
CARONLESLIE LAM; EVANS RB; CIDLOWSKI JA;
Indirizzi:
UNIV N CAROLINA,DEPT PHYSIOL,460 MED SCI RES BLDG,CB 7545 CHAPEL HILLNC 27599 UNIV N CAROLINA,DEPT PHYSIOL CHAPEL HILL NC 27599 UNIV N CAROLINA,LINEBERGER CANC RES CTR CHAPEL HILL NC 27599
Titolo Testata:
The FASEB journal
fascicolo: 9, volume: 8, anno: 1994,
pagine: 639 - 645
SICI:
0892-6638(1994)8:9<639:BIGABO>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
DNA FRAGMENTATION; THYMOCYTE APOPTOSIS; PROTEIN-SYNTHESIS; DEATH APOPTOSIS; LYMPHOMA-CELLS; GENE; INVOLVEMENT; EXPRESSION; SELECTION; SURVIVAL;
Keywords:
DEXAMETHASONE; PROGRAMMED CELL DEATH; STEROID; ANTIPROLIFERATION; BCL-2 EXPRESSION; INTERNUCLEOSOMAL DNA DEGRADATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
29
Recensione:
Indirizzi per estratti:
Citazione:
L.A.M. Caronleslie et al., "BCL-2 INHIBITS GLUCOCORTICOID-INDUCED APOPTOSIS BUT ONLY PARTIALLY BLOCKS CALCIUM IONOPHORE OR CYCLOHEXIMIDE-REGULATED APOPTOSIS IN S49 CELLS", The FASEB journal, 8(9), 1994, pp. 639-645

Abstract

Many non-Hodgkins B-cell lymphomas possess a deregulated bcl-2 gene resulting in a phenotype that is apparently resistant to programmed eeldeath (apoptosis). We have used a mouse lymphoma cell line (S49.1) that undergoes apoptosis in response to a variety of stimuli to determine the effect of bcl-2 expression on induction of apoptosis. S49 cells were stably transfected with recombinant amphotrophic retroviruses carrying either a G418 antibiotic resistance gene alone (S49-NEO) or thisgene in combination with a bcl-2 complementary DNA (S49-Bcl-2). Threedifferent agents previously shown to activate apoptosis by different pathways in S49 cells (dexamethasone, the calcium ionophore A23187, and cycloheximide) were used to examine the effect of bcl-2 expression on cell growth and apoptosis caused by multiple signal transduction pathways. Dexamethasone (DEX) treatment inhibited cell growth and stimulated cell death in S49-NEO cells. Although S49-Bcl-2 cells exhibited a similar antiproliferative response, they failed to die in response to steroid treatment. Western blot analysis revealed no difference in thelevels of glucocorticoid receptor protein in the two cell lines, and both responded to glucocorticoid with a profound inhibition of proteinsynthesis. Cycloheximide (CX) and A23187 also had antiproliferative and cell killing effects in both cell types, although higher concentrations of each agent were needed to kill S49-Bcl-2 cells. To determine whether the loss of viability in response to these drugs was due to apoptosis, cells were examined morphologically and DNA integrity was examined by gel electrophoresis. The presence of condensed chromatin and an internucleosomal pattern of DNA degradation was used as an index of apoptosis. The S49-NEO cells exhibited internucleosomal DNA degradation and an apoptotic morphology in response to DEX, A23187, and CX treatment, indicating that these compounds cause apoptotic death in this cell type. Similar internucleosomal DNA degradation and cellular morphology were observed in A23187- and CX-treated S49-Bcl-2 cells, but not in the DEX-treated S49-Bcl-2 cells. These data indicate that Bcl-2 doesnot interfere with the mechanisms responsible for apoptosis, but rather alters signaling pathways controlling its activation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 17:25:49