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Transmembrane protein 166 regulates autophagic and apoptotic activities following focal cerebral ischemic injury in rats
Li, Li1; Khatibi, Nikan H.2; Hu, Qin1,3; Yan, Junhao1,3; Chen, Chunhua1,3; Han, Jingyan4; Ma, Dalong5; Chen, Yinyu5; Zhou, Changman1
关键词Autophagy Apoptosis TMEM166 Cerebral ischemia MCAO
刊名EXPERIMENTAL NEUROLOGY
2012-03-01
DOI10.1016/j.expneurol.2011.12.038
234期:1页:181-190
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Neurosciences
研究领域[WOS]Neurosciences & Neurology
关键词[WOS]CELL-DEATH ; ARTERY OCCLUSION ; HYPOXIA-ISCHEMIA ; BRAIN-INJURY ; BCL-2 ; DEGRADATION ; HEMORRHAGE ; NEURONS ; GENE
英文摘要

Transmembrane protein 166 (TMEM166) is a lysosomal/endoplasmic reticulum-associated protein found in various species where it acts as a regulator of programmed cell death, mediating both autophagy and apoptosis. In the present study, we investigated the role of TMEM166 following MCAO injury in rats to determine whether the structural damages following injury were orchestrated in part by TMEM166. One hundred and fifty six male Sprague-Dawley rats were randomly divided into 4 groups: Sham, MCAO, MCAO + control siRNA, MCAO + TMEM166 siRNA. Outcomes were measured including mortality rate, brain edema, BBB disruption, and neurobehavioral testing. Western blotting techniques measured the expression of key proautophagic and apoptotic proteins such as TMEM166. Beclin-1, cleaved casepase-3 and Bcl-2/Bax. The study found that TMEM166 siRNA treatment significantly reduced the mortality rate, cerebral edema, neurobehavioral deficits, and BBB disruption as measured by Evan′s blue assay following MCAO injury. Immunohistochemical staining and western blotting analysis demonstrated an increased expressions of TMEM166, Beclin-1, LC3, cleaved casepase-3 and Bcl-2/Bax in the infarcted areas. This study suggests that TMEM166 induces autophagy and apoptosis may in fact play a significant role in cell death following MCAO injury and its mediation may be through the crosstalk of Bcl-2. By blocking the activity of TMEM166 using siRNA, we were able to prevent the cell loss that occured following cerebral ischemia injury. This translated into a preservation of functional integrity and an improvement in mortality. (C) 2012 Elsevier Inc. All rights reserved.

语种英语
WOS记录号WOS:000301617500020
项目编号2011 CB910103 ; 30971527
资助机构National Key Project for Basic Research of China ; National Natural Science Foundation of China
引用统计
被引频次:21[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/62856
专题北京大学基础医学院
作者单位1.Loma Linda Med Ctr, Dept Anesthesiol, Loma Linda, CA USA
2.Peking Univ, Dept Anat & Histol, Sch Basic Med Sci, Hlth Sci Ctr, Beijing 100191, Peoples R China
3.Loma Linda Med Ctr, Dept Neurosurg, Loma Linda, CA USA
4.Peking Univ, Hlth Sci Ctr, Microcirculat Res Ctr, Beijing 100191, Peoples R China
5.Peking Univ, Hlth Sci Ctr, Minist Hlth, Key Lab Med Immunol, Beijing 100191, Peoples R China
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GB/T 7714
Li, Li,Khatibi, Nikan H.,Hu, Qin,et al. Transmembrane protein 166 regulates autophagic and apoptotic activities following focal cerebral ischemic injury in rats[J]. EXPERIMENTAL NEUROLOGY,2012,234(1):181-190.
APA Li, Li.,Khatibi, Nikan H..,Hu, Qin.,Yan, Junhao.,Chen, Chunhua.,...&Zhou, Changman.(2012).Transmembrane protein 166 regulates autophagic and apoptotic activities following focal cerebral ischemic injury in rats.EXPERIMENTAL NEUROLOGY,234(1),181-190.
MLA Li, Li,et al."Transmembrane protein 166 regulates autophagic and apoptotic activities following focal cerebral ischemic injury in rats".EXPERIMENTAL NEUROLOGY 234.1(2012):181-190.
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