Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8277989 | Journal of the Neurological Sciences | 2014 | 13 Pages |
Abstract
We found that 1) Smad1, -2, -3, and -5 proteins were detected in the rat hippocampus by means of western blot and immunohistochemistry; 2) after 5Â min of ischemia, Smad2 and Smad3 proteins accumulated in the nuclei of pyramidal cells in the CA1 region, which is vulnerable to ischemia; 3) after 3Â min of ischemia, which was non-lethal, there was no such nuclear accumulation of Smad2 and Smad3 in the CA1 region; 4) following injection of activin A, nuclear accumulation of Smad2 and Smad3 was induced not only in pyramidal cells of the CA1 region, but also in pyramidal cells of the CA3 region as well as in granule cells of the DG region; 5) activin A-induced nuclear accumulation of Smad2 and Smad3 neither caused degeneration of hippocampal neurons nor prevented degeneration induced by ischemia. These results suggest that in the hippocampus, ischemia-induced activation of Smad2 and Smad3 is associated with the response to stress but is not related to neuronal survival or death.
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Authors
Takayuki Nakajima, Masafumi Yanagihara, Hideki Nishii,