Journal
JOURNAL OF NEUROSCIENCE
Volume 29, Issue 36, Pages 11385-11392Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4780-08.2009
Keywords
-
Categories
Funding
- Japanese Ministry of Education, Science, Sports, Culture, and Technology
- RIKEN Bioarchitect Research
- Japan Society for the Promotion of Science for Young Scientists
- Grants-in-Aid for Scientific Research [19109003] Funding Source: KAKEN
Ask authors/readers for more resources
Caspases are essential in multicellular organisms for inducing cell death during normal development and in the immune system. However, caspases can also trigger the degenerative process under certain conditions such as pathophysiological conditions and aging. Here, we identified Semaphorin7A (Sema7A) as a novel substrate for caspase-9 that can be used to monitor caspase-9 activity in mice, and found nonapoptotic caspase-9 activation in the aged olfactory bulb (OB). Immunostaining of the OB for the caspase-9-cleaved form of Sema7A revealed abundant caspase-9-activated cells in 2-year-old (aged) but not in 2-month-old (young) mice. In fact, various regions of the aged brain, including the OB, exhibited an increased level of caspase-9 activity. However, the number of dying cells in the aged OB was, intriguingly, much lower (<20%) than in the OB of young mice. Furthermore, we found that the lower number dying cells in the aged OB was accompanied by a decreased expression of procaspase-3. These results suggest a survival strategy for aged OB neurons, which can no longer regenerate, in which the central apoptotic machinery downstream of caspase-9 is inactivated.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available