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学科主题: 基础医学
题名:
The Involvement of Programmed Cell Death 5 (PDCD5) in the Regulation of Apoptosis in Cerebral Ischemia/Reperfusion Injury
作者: Chen, Chun-Hua1; Jiang, Zhao1; Yan, Jun-Hao1; Yang, Lei1; Wang, Ke1; Chen, Ying-Yu2; Han, Jing-Yan3; Zhang, John H.4; Zhou, Chang-Man1
关键词: Apoptosis ; MCAO ; PDCD5 ; siRNA in vivo
刊名: CNS NEUROSCIENCE & THERAPEUTICS
发表日期: 2013-08-01
DOI: 10.1111/cns.12114
卷: 19, 期:8, 页:566-576
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Neurosciences ; Pharmacology & Pharmacy
研究领域[WOS]: Neurosciences & Neurology ; Pharmacology & Pharmacy
关键词[WOS]: GENE-EXPRESSION PROFILES ; ARTERY OCCLUSION ; HYPERBARIC-OXYGEN ; TUMOR-CELLS ; RAT MODEL ; INTERFERING RNA ; BRAIN-INJURY ; DNA-DAMAGE ; ISCHEMIA ; NEUROPROTECTION
英文摘要:

AimsProgrammed Cell Death 5 (PDCD5) is a protein that accelerates apoptosis in different types of cells in response to various stimuli and is down-regulated in many cancer tissues. We hypothesized in this study that down-regulating PDCD5 can protect the brain from ischemic damage by inhibiting PDCD5-induced apoptotic pathway.

MethodsOne hundred and sixty male Sprague-Dawley rats were randomly assigned to five groups: Sham surgery (n=25), MCAO (n=45), MCAO+rhPDCD5 (RhPDCD5) (n=30), MCAO+control siRNA (n=30), and MCAO+PDCD5 siRNA (n=30). At 24h following MCAO, immunohistochemistry and Western blot were performed.

ResultsPDCD5 siRNA reduced the infarct volume, improved neurological deficits, improved cerebral blood flow (CBF), and reduced Evans blue extravasation. Meanwhile, over-expression of PDCD5 protein with recombinant human PDCD5 (rhPDCD5) had an opposite effect. Immunohistochemistry and Western blot demonstrated PDCD5 siRNA decreased the expressions of key proapoptotic proteins such as p53, Bax/Bcl-2, and cleaved caspase-3 in the penumbra areas, whereas rhPDCD5 increased cell apoptosis. Double fluorescence labeling showed the positive immunoreactive materials of PDCD5 were partly colocalized with MAP2, GFAP, CD34, p53, and caspase-3 in the penumbra areas in brain.

ConclusionsPDCD5-induced apoptosis and over-expression of PDCD5 are harmful to the ischemic neurons in vivo. Meanwhile, the inhibition of PDCD5 may be protective via reducing the apoptotic-related protein such as p53, Bax, and caspase-3. This observation may have potential for the treatment of ischemic cerebral stroke.

语种: 英语
所属项目编号: 81000523 ; 31271280
项目资助者: National Natural Science Foundation of China
WOS记录号: WOS:000328288400004
Citation statistics:
内容类型: 期刊论文
版本: 出版稿
URI标识: http://ir.bjmu.edu.cn/handle/400002259/63997
Appears in Collections:基础医学院_北京大学人类疾病基因研究中心_期刊论文

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作者单位: 1.Peking Univ, Dept Anat & Embryol, Hlth Sci Ctr, Beijing 100191, Peoples R China
2.Peking Univ, Ctr Human Dis Genom, Beijing 100191, Peoples R China
3.State Adm Tradit Chinese Med, Key Lab Stasis & Phlegm, Beijing, Peoples R China
4.Loma Linda Univ, Dept Neurosurg, Loma Linda, CA 92350 USA

Recommended Citation:
Chen, Chun-Hua,Jiang, Zhao,Yan, Jun-Hao,et al. The Involvement of Programmed Cell Death 5 (PDCD5) in the Regulation of Apoptosis in Cerebral Ischemia/Reperfusion Injury[J]. CNS NEUROSCIENCE & THERAPEUTICS,2013,19(8):566-576.
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