Neurological research · 2010
Cyclin D1 immunoreactivity changes in CA1 pyramidal neurons and dentate granule cells in the gerbil hippocampus after transient forebrain ischemia.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Lee Choong Hyun, Yoo Ki-Yeon, Choi Jung Hoon, Park Ok Kyu, Hwang In Koo, Choi Soo Young, Kim Do-Hoon, Won Moo-Ho
Аннотация
OBJECTIVES: Cyclin D1, a member of the G1 cyclin family, plays a critical role in the progression of the cell cycle. In the present study, we investigated chronological alterations in cyclin D1 immunoreactivity and its protein levels in the gerbil hippocampus after ischemia/reperfusion.
METHODS: Chronological alterations in cyclin D1 immunoreactivity and its levels were examined in the gerbil hippocampus after ischemia/reperfusion using immunohistochemistry and western blot analysis.
RESULTS: Changes in cyclin D1 immunoreactivity in the ischemic hippocampus were distinct in pyramidal neurons of the CA1 region and granule cells of the dentate gyrus. Cyclin D1 immunoreactivity in pyramidal neurons of the CA1 region was increased up to 1 day after ischemia/reperfusion, although a transient decrease of cyclin D1 immunoreactivity was detected at 12 hour after ischemia/reperfusion. Thereafter, cyclin D1 immunoreactivity in the CA1 pyramidal neurons was very weak 2 days and disappeared nearly 4 and 7 days after ischemia/reperfusion. However, 4 days after ischemia/reperfusion, the cyclin D1 immunoreactivity in non-pyramidal neurons of the CA1 region was very strong. In the CA2/3 region, cyclin D1 immunoreactivity was higher than that in the CA1 region and not changed after ischemia/reperfusion. In the dentate gyrus, chronological change in cyclin D1 immunoreactivity was observed. Cells in the granule cell layer showed distinct change in cyclin D1 immunoreactivity after ischemia/reperfusion: the cyclin D1 immunoreactivity was lowest at 12 hours and strong 1 and 4 days after ischemia/reperfusion. In addition, change in cyclin D1 protein level was found in the ischemic hippocampus.
CONCLUSION: Our results indicate that cyclin D1 may play an important role in cellular events related with neuronal damage following ischemia/reperfusion.
METHODS: Chronological alterations in cyclin D1 immunoreactivity and its levels were examined in the gerbil hippocampus after ischemia/reperfusion using immunohistochemistry and western blot analysis.
RESULTS: Changes in cyclin D1 immunoreactivity in the ischemic hippocampus were distinct in pyramidal neurons of the CA1 region and granule cells of the dentate gyrus. Cyclin D1 immunoreactivity in pyramidal neurons of the CA1 region was increased up to 1 day after ischemia/reperfusion, although a transient decrease of cyclin D1 immunoreactivity was detected at 12 hour after ischemia/reperfusion. Thereafter, cyclin D1 immunoreactivity in the CA1 pyramidal neurons was very weak 2 days and disappeared nearly 4 and 7 days after ischemia/reperfusion. However, 4 days after ischemia/reperfusion, the cyclin D1 immunoreactivity in non-pyramidal neurons of the CA1 region was very strong. In the CA2/3 region, cyclin D1 immunoreactivity was higher than that in the CA1 region and not changed after ischemia/reperfusion. In the dentate gyrus, chronological change in cyclin D1 immunoreactivity was observed. Cells in the granule cell layer showed distinct change in cyclin D1 immunoreactivity after ischemia/reperfusion: the cyclin D1 immunoreactivity was lowest at 12 hours and strong 1 and 4 days after ischemia/reperfusion. In addition, change in cyclin D1 protein level was found in the ischemic hippocampus.
CONCLUSION: Our results indicate that cyclin D1 may play an important role in cellular events related with neuronal damage following ischemia/reperfusion.