Suppr超能文献

沙土鼠全脑短暂缺血后海马本部神经元和胶质细胞中Redd1的变化及表达

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

作者信息

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

机构信息

Department of Pharmacy, College of Pharmacy, Dankook University, Cheonan 330-714, South Korea.

Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea.

出版信息

J Neurol Sci. 2014 Sep 15;344(1-2):43-50. doi: 10.1016/j.jns.2014.06.016. Epub 2014 Jun 19.

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.

摘要

Redd1(也称为RTP801/Dig2/DDIT4)是一种应激诱导蛋白,已知其表达受包括缺氧和氧化应激在内的某些应激反应调控。在本研究中,我们采用免疫组织化学和蛋白质印迹分析方法,研究了沙土鼠全脑短暂缺血5分钟后,其海马本部(CA1 - 3区)Redd1免疫反应性及其蛋白水平随时间的变化。缺血CA1区的锥体神经元中Redd1免疫反应性明显改变,而缺血CA2/3区的锥体神经元中则未改变。CA1锥体神经元中的Redd1免疫反应性在缺血后6小时显著增加,至缺血后1天下降,缺血后2天再次升高,在缺血后5天微弱表达。特别值得注意的是,在缺血损伤5天后,CA1区的星形胶质细胞和GABA能中间神经元中新出现了Redd1免疫反应性。缺血CA1区的Redd1蛋白水平变化与Redd1免疫反应性模式一致。这些结果表明,在缺血损伤后的早期,缺血CA1区的Redd1免疫反应性和蛋白水平升高,且Redd1表达的增加可能与全脑短暂缺血5分钟后CA1锥体神经元的延迟性神经元死亡密切相关。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验