Ischemia-Induced Changes of PRAS40 and p-PRAS40 Immunoreactivities in the Gerbil Hippocampal CA1 Region After Transient Cerebral Ischemia |
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| Authors: | Joon Ha Park Bich Na Shin Ji Hyeon Ahn Jeong-Hwi Cho In Hye Kim Dae Won Kim Moo-Ho Won Seongkweon Hong Jun Hwi Cho Choong-Hyun Lee |
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| Institution: | 1.Department of Neurobiology, School of Medicine,Kangwon National University,Chuncheon,South Korea;2.Department of Physiology, College of Medicine,Hallym University,Chuncheon,South Korea;3.Department of Biochemistry and Molecular Biology, College of Dentistry, and Research Institute of Oral Sciences,Kangnung-Wonju National University,Gangneung,South Korea;4.Department of Surgery, School of Medicine,Kangwon National University,Chuncheon,South Korea;5.Department of Emergency Medicine, College of Medicine, School of Medicine,Kangwon National University,Chuncheon,South Korea;6.Department of Pharmacy, College of Pharmacy,Dankook University,Cheonan,South Korea |
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| Abstract: | Proline-rich Akt substrate of 40-kDa (PRAS40) is one of the important interactive linkers between Akt and mTOR signaling pathways. The increase of PRAS40 is related with the reduction of brain damage induced by cerebral ischemia. In the present study, we investigated time-dependent changes in PRAS40 and phospho-PRAS40 (p-PRAS40) immunoreactivities in the hippocampal CA1 region of the gerbil after 5 min of transient cerebral ischemia. PRAS40 immunoreactivity in the CA1 region was decreased in pyramidal neurons from 12 h after ischemic insult in a time-dependent manner, and, at 5 days post-ischemia, PRAS40 immunoreactivity was newly expressed in astrocytes. p-PRAS40 immunoreactivity in the CA1 pyramidal neurons was hardly found 12 h and apparently detected again 1 and 2 days after ischemic insult. At 5 days post-ischemia, p-PRAS40 immunoreactivity in the CA1 pyramidal neurons was not found. These results indicate that ischemia-induced changes in PRAS40 and p-PRAS40 immunoreactivities in CA1 pyramidal neurons and astrocytes may be closely associated with delayed neuronal death in the hippocampal CA1 region following transient cerebral ischemia. |
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