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

Choong Hyun Lee, Joon Ha Park, Jeong Hwi Cho, Ji Hyeon Ahn, Bing Chun Yan, Jae Chul Lee, Myoung Cheol Shin, Seung Hwan Cheon, Young Shin Cho, Jun Hwi Cho, Young Guen Kwon, Dong Keon Lee, Young Myeong Kim, Moo Ho Won

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)43-50
Number of pages8
JournalJournal of the Neurological Sciences
Volume344
Issue number1-2
DOIs
Publication statusPublished - 2014 Sep 15

Bibliographical note

Funding Information:
The authors would like to thank Mr. Seung Uk Lee for his technical help. This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by xthe Ministry of Science, ICT & Future Planning (NRF-2012R1A1A1007298), and by the National Research Foundation of Korea (NRF) Grant funded by the Korea government (MEST) (2011-0028790).

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology

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