北京大学医学部机构知识库
Advanced  
IR@PKUHSC  > 基础医学院  > 期刊论文
学科主题: 基础医学
题名:
Transmembrane protein 166 regulates autophagic and apoptotic activities following focal cerebral ischemic injury in rats
作者: 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
发表日期: 2012-03-01
DOI: 10.1016/j.expneurol.2011.12.038
卷: 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
所属项目编号: 2011 CB910103 ; 30971527
项目资助者: National Key Project for Basic Research of China ; National Natural Science Foundation of China
WOS记录号: WOS:000301617500020
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/62856
Appears in Collections:基础医学院_期刊论文

Files in This Item:

There are no files associated with this item.


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

Recommended Citation:
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.
Service
Recommend this item
Sava as my favorate item
Show this item's statistics
Export Endnote File
Google Scholar
Similar articles in Google Scholar
[Li, Li]'s Articles
[Khatibi, Nikan H.]'s Articles
[Hu, Qin]'s Articles
CSDL cross search
Similar articles in CSDL Cross Search
[Li, Li]‘s Articles
[Khatibi, Nikan H.]‘s Articles
[Hu, Qin]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Copyright © 2007-2017  北京大学医学部 - Feedback
Powered by CSpace