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Bcl-2-linked apoptosis due to increase in NO synthase in brain of SAMP10
- Source :
-
Biochemical & Biophysical Research Communications . Sep2002, Vol. 297 Issue 3, p517. 6p. - Publication Year :
- 2002
-
Abstract
- We examined the linkage of nitric oxide (NO)-induced apoptosis to acceleration of brain aging of senescence-accelerated mouse prone 10 (SAMP10). The expression of neuronal nitric oxide synthase (nNOS) increased in the cerebral cortex of the brain of SAMP10 in an age-dependent manner and significantly higher levels of neuronal nitric oxide synthase (nNOS) were observed in both young and old SAMP10 as compared to age-matched controls. Moreover, a lower level of anti-apoptotic protein Bcl-2 and a higher level of pro-apoptotic protein cytochrome <f>c</f> in cytosol were observed in SAMP10 compared to the control. However, there was no significant difference in the expression of pro-apoptotic protein p53 between SAMP10 and the control. Furthermore, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL)-positive apoptotic cells were more abundant in the cerebral cortex of aged SAMP10 than in the control. The present results suggest that an age-dependent increase of NO by up-regulation of nNOS promotes the Bcl-2-linked apoptosis in the cerebral cortex of SAMP10 and this may cause the acceleration of brain aging of SAMP10. [Copyright &y& Elsevier]
- Subjects :
- *NITRIC oxide
*APOPTOSIS
*BRAIN
*AGING
Subjects
Details
- Language :
- English
- ISSN :
- 0006291X
- Volume :
- 297
- Issue :
- 3
- Database :
- Academic Search Index
- Journal :
- Biochemical & Biophysical Research Communications
- Publication Type :
- Academic Journal
- Accession number :
- 8516042
- Full Text :
- https://doi.org/10.1016/S0006-291X(02)02155-1