学科主题基础医学
Autophagic effect of programmed cell death 5 (PDCD5) after focal cerebral ischemic reperfusion injury in rats
Jiang, Zhao1; Chen, Chun-Hua1; Chen, Ying-Yu2; Han, Jing-Yan3; Riley, John4; Zhou, Chang-Man1
关键词MCAO PDCD5 Autophagy MRI siRNA
刊名NEUROSCIENCE LETTERS
2014-04-30
DOI10.1016/j.neulet.2014.02.066
566期:0页:298-303
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]DOUBLE-EDGED-SWORD ; ARTERY OCCLUSION ; HYPERBARIC-OXYGEN ; INDUCED APOPTOSIS ; MODEL ; INHIBITION ; PROTEINS ; BECLIN-1
英文摘要

Former studies indicated that programmed cell death 5 (PDCD5) protein could accelerate the process of apoptosis in response to some stimuli in various kinds of cells via the intrinsic or extrinsic pathway. In this study, we aimed to demonstrate for the first time that protein level of PDCD5 are related to autophagic activity after focal ischemic brain injury in rats. One hundred and twenty-five Sprague-Dawley rats (male) were randomly divided into the following groups: Sham operated, Middle Cerebral Artery Occlusion/Reperfusion (MCAO), MCAO + Control siRNA and MCAO + PDCD5 siRNA. Outcome measurements include neurobehavioral outcomes, brain infarct volume, brain water content, BBB disruption, MRI and double fluorescence labeling. Western blot and histopathophysiological techniques were used to measure the expression of PDCD5 and some pro-autophagic proteins such as Beclin 1 and the LC3-II/LC3-I ratio. The study found that decreased PDCD5 expression via intracerebroventricular injection of PDCD5 siRNA significantly improved the neurobehavioral outcome, reduced the infarct ratio, cerebral edema and BBB disruption. These results were associated with decreased expression of Beclin 1 and the LC3-II/LC3-I ratio in the penumbra area. Rapamycin, an inducer of autophagy, partially weakened the effect of PDCD5 siRNA. In conclusion, this study suggested that PDCD5 was a key regulator of autophagy that might play an important role following MCAO injury. (C) 2014 Elsevier Ireland Ltd. All rights reserved.

语种英语
WOS记录号WOS:000335613800058
项目编号81000523 ; 31271280
资助机构National Natural Science Foundation of China
引用统计
被引频次:12[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/55185
专题北京大学基础医学院_北京大学人类疾病基因研究中心
北京大学基础医学院
作者单位1.Peking Univ, Hlth Sci Ctr, Dept Anatomyand Embryol, Beijing 100191, Peoples R China
2.Peking Univ, Ctr Human Dis Genom, Beijing 100871, Peoples R China
3.State Adm Tradit Chinese Med, Key Lab Stasis & Phlegm, Beijing, Peoples R China
4.Hosp Univ Penn, Dept Anesthesiol & Crit Care, Philadelphia, PA 19104 USA
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GB/T 7714
Jiang, Zhao,Chen, Chun-Hua,Chen, Ying-Yu,et al. Autophagic effect of programmed cell death 5 (PDCD5) after focal cerebral ischemic reperfusion injury in rats[J]. NEUROSCIENCE LETTERS,2014,566(0):298-303.
APA Jiang, Zhao,Chen, Chun-Hua,Chen, Ying-Yu,Han, Jing-Yan,Riley, John,&Zhou, Chang-Man.(2014).Autophagic effect of programmed cell death 5 (PDCD5) after focal cerebral ischemic reperfusion injury in rats.NEUROSCIENCE LETTERS,566(0),298-303.
MLA Jiang, Zhao,et al."Autophagic effect of programmed cell death 5 (PDCD5) after focal cerebral ischemic reperfusion injury in rats".NEUROSCIENCE LETTERS 566.0(2014):298-303.
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