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Titolo:
APOPTOSIS OF BCL-X-DEFICIENT TELENCEPHALIC CELLS IN-VITRO
Autore:
ROTH KA; MOTOYAMA N; LOH DY;
Indirizzi:
WASHINGTON UNIV,SCH MED,DEPT PATHOL,CAMPUS BOX 8118 ST LOUIS MO 63110 WASHINGTON UNIV,SCH MED,DEPT MOLEC BIOL & PHARMACOL ST LOUIS MO 63110 WASHINGTON UNIV,SCH MED,HOWARD HUGHES MED INST ST LOUIS MO 63110 WASHINGTON UNIV,SCH MED,DEPT MED ST LOUIS MO 63110 WASHINGTON UNIV,SCH MED,DEPT GENET ST LOUIS MO 63110 WASHINGTON UNIV,SCH MED,DEPT MOLEC MICROBIOL ST LOUIS MO 63110
Titolo Testata:
The Journal of neuroscience
fascicolo: 5, volume: 16, anno: 1996,
pagine: 1753 - 1758
SICI:
0270-6474(1996)16:5<1753:AOBTCI>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
NERVOUS-SYSTEM; CEREBRAL-CORTEX; DEATH; REMOVAL; MOUSE; ZONE; RAT;
Keywords:
APOPTOSIS; PROGRAMMED CELL DEATH; BCL-X; BCL-2; NEURONAL DEVELOPMENT; NEUROPROTECTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Physical, Chemical & Earth Sciences
Science Citation Index Expanded
Citazioni:
33
Recensione:
Indirizzi per estratti:
Citazione:
K.A. Roth et al., "APOPTOSIS OF BCL-X-DEFICIENT TELENCEPHALIC CELLS IN-VITRO", The Journal of neuroscience, 16(5), 1996, pp. 1753-1758

Abstract

bcl-x is a member of the bcl-2 gene family, which is expressed at high levels in the embryonic brain. The targeted disruption of bcl-x results in massive cell death of immature neurons in the developing mouse brain (Motoyama et al., 1995). bcl-x-deficient mice die around embryonic day 13 (E13), probably secondary to their inability to produce mature red blood cells. To determine whether the death of immature neuronsin the bcl-x-deficient brain is cell autonomous, we examined primary telencephalic cell cultures from E12.5 homozygous mutant (bcl-x(-/-)),heterozygous mutant (bcl-x(+/-)), and wild-type (bcl-x(+/+)) mice, bcl-x(-/-) telencephalic cells cultured in 0.5 or 2.0% fetal calf serum (FCS)-containing medium for 48 hr showed increased apoptosis, defined by abnormal bisbenzamide staining and terminal-deoxytransferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL), and decreased numbers of microtubule-associated protein-2-immunoreactive neurons compared with bcl-x(+/-) and bcl-x(+/+) cultures. Cycloheximide treatmentof bcl-x(-/-) telencephalic cell cultures failed to prevent the increased cell death observed in low FCS-containing medium, suggesting a protein synthesis-independent apoptosis. There were no significant differences among bcl-x(-/-), bcl-x(+/-), and bcl-x(+/+) telencephalic cells grown for 48 hr in 5% FCS-containing medium or in a chemically defined serum-free medium (ITS). bcl-x(-/-) neurons generated in ITS showedin creased susceptibility to subsequent serum deprivation. These results indicate that bcl-x is important for both neuron maturation and survival.

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Documento generato il 07/07/20 alle ore 17:44:17