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OT-II转基因小鼠的记忆受损与成年海马神经发生减少有关,这可能是由Th2细胞因子水平改变所致。

Impaired Memory in OT-II Transgenic Mice Is Associated with Decreased Adult Hippocampal Neurogenesis Possibly Induced by Alteration in Th2 Cytokine Levels.

作者信息

Jeon Seong Gak, Kim Kyoung Ah, Chung Hyunju, Choi Junghyun, Song Eun Ji, Han Seung-Yun, Oh Myung Sook, Park Jong Hwan, Kim Jin-Il, Moon Minho

机构信息

Department of Biochemistry, College of Medicine, Konyang University, Dajeon 35365, Korea.

Department of Core Research Laboratory, Clinical Research Institute, Kyung Hee University Hospital at Gangdong, Seoul 0527, Korea.

出版信息

Mol Cells. 2016 Aug 31;39(8):603-10. doi: 10.14348/molcells.2016.0072. Epub 2016 Jul 19.

DOI:10.14348/molcells.2016.0072
PMID:27432189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4990752/
Abstract

Recently, an increasing number of studies have focused on the effects of CD4+ T cell on cognitive function. However, the changes of Th2 cytokines in restricted CD4+ T cell receptor (TCR) repertoire model and their effects on the adult hippocampal neurogenesis and memory are not fully understood. Here, we investigated whether and how the mice with restricted CD4+ repertoire TCR exhibit learning and memory impairment by using OT-II mice. OT-II mice showed decreased adult neurogenesis in hippocampus and short- and long- term memory impairment. Moreover, Th2 cytokines in OT-II mice are significantly increased in peripheral organs and IL-4 is significantly increased in brain. Finally, IL-4 treatment significantly inhibited the proliferation of cultured adult rat hippocampal neural stem cells. Taken together, abnormal level of Th2 cytokines can lead memory dysfunction via impaired adult neurogenesis in OT-II transgenic.

摘要

最近,越来越多的研究聚焦于CD4+ T细胞对认知功能的影响。然而,在受限的CD4+ T细胞受体(TCR)库模型中Th2细胞因子的变化及其对成年海马神经发生和记忆的影响尚未完全明确。在此,我们利用OT-II小鼠研究了具有受限TCR库的CD4+小鼠是否以及如何表现出学习和记忆障碍。OT-II小鼠表现出海马区成年神经发生减少以及短期和长期记忆障碍。此外,OT-II小鼠外周器官中的Th2细胞因子显著增加,大脑中的IL-4显著增加。最后,IL-4处理显著抑制了培养的成年大鼠海马神经干细胞的增殖。综上所述,Th2细胞因子水平异常可通过OT-II转基因小鼠成年神经发生受损导致记忆功能障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ada/4990752/87c6c09a0232/molce-39-8-603f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ada/4990752/caf0dbf8fe16/molce-39-8-603f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ada/4990752/21a61658c38a/molce-39-8-603f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ada/4990752/05d391e821bc/molce-39-8-603f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ada/4990752/c0b11bb639b8/molce-39-8-603f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ada/4990752/87c6c09a0232/molce-39-8-603f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ada/4990752/caf0dbf8fe16/molce-39-8-603f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ada/4990752/eaeaa2a1c61d/molce-39-8-603f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ada/4990752/21a61658c38a/molce-39-8-603f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ada/4990752/05d391e821bc/molce-39-8-603f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ada/4990752/c0b11bb639b8/molce-39-8-603f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ada/4990752/87c6c09a0232/molce-39-8-603f6.jpg

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