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      Changes and expressions of Redd1 in neurons and glial cells in the gerbil hippocampus proper following transient global cerebral ischemia.

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          Abstract

          Redd1 (known as RTP801/Dig2/DDIT4) is a stress-induced protein, and it is known to be regulated in response to some stresses including hypoxia and oxidative stress. In the present study, we investigated the time-dependent changes in Redd1 immunoreactivity and its protein levels in the gerbil hippocampus proper (CA1-3 regions) after 5 min of transient global cerebral ischemia using immunohistochemistry and Western blot analysis. Redd1 immunoreactivity was apparently changed in the pyramidal neurons of the ischemic CA1 region, not in the pyramidal neurons of the ischemic CA2/3 region. Redd1 immunoreactivity in the CA1 pyramidal neurons was significantly increased at 6 h post-ischemia, decreased until 1 day post-ischemia, increased again at 2 days post-ischemia and weakly observed at 5 days post-ischemia. Especially, at 5 days after ischemic damage, Redd1 immunoreactivity was newly expressed in astrocytes and GABAergic interneurons in the CA1 region. Redd1 protein levels in the ischemic CA1 region were changed like the pattern of the Redd1 immunoreactivity. These results indicate that Redd1 immunoreactivity and protein levels are increased in the ischemic CA1 region at an early time after ischemic damage and that the increased Redd1 expression may be closely related to the delayed neuronal death of the CA1 pyramidal neurons following 5 min of transient global cerebral ischemia.

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          Author and article information

          Journal
          J. Neurol. Sci.
          Journal of the neurological sciences
          1878-5883
          0022-510X
          Sep 15 2014
          : 344
          : 1-2
          Affiliations
          [1 ] Department of Pharmacy, College of Pharmacy, Dankook University, Cheonan 330-714, South Korea.
          [2 ] Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea.
          [3 ] Department of Integrative Traditional & Western Medicine, Medical College, Yangzhou University, Yangzhou, Jiangsu 225001, China.
          [4 ] Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea.
          [5 ] Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea; Department of Emergency Medicine, Seoul Hospital, College of Medicine, Sooncheonhyang University, Seoul 140-743, South Korea.
          [6 ] Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 120-749, South Korea.
          [7 ] Department of Molecular and Cellular Biochemistry, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea.
          [8 ] Department of Molecular and Cellular Biochemistry, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea. Electronic address: ymkim@kangwon.ac.kr.
          [9 ] Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea. Electronic address: mhwon@kangwon.ac.kr.
          Article
          S0022-510X(14)00386-4
          10.1016/j.jns.2014.06.016
          24980938
          431da52c-e18e-4166-99c1-1e232454e6e7
          Copyright © 2014 Elsevier B.V. All rights reserved.
          History

          Astrocyte,CA1 pyramidal neurons,Delayed neuronal death,GABAergic interneurons,Redd1,Transient global cerebral ischemia

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