学科主题基础医学
The Involvement of Programmed Cell Death 5 (PDCD5) in the Regulation of Apoptosis in Cerebral Ischemia/Reperfusion Injury
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
2013-08-01
DOI10.1111/cns.12114
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
WOS记录号WOS:000328288400004
项目编号81000523 ; 31271280
资助机构National Natural Science Foundation of China
引用统计
被引频次:31[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/400002259/63997
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, 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
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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.
APA Chen, Chun-Hua.,Jiang, Zhao.,Yan, Jun-Hao.,Yang, Lei.,Wang, Ke.,...&Zhou, Chang-Man.(2013).The Involvement of Programmed Cell Death 5 (PDCD5) in the Regulation of Apoptosis in Cerebral Ischemia/Reperfusion Injury.CNS NEUROSCIENCE & THERAPEUTICS,19(8),566-576.
MLA Chen, Chun-Hua,et al."The Involvement of Programmed Cell Death 5 (PDCD5) in the Regulation of Apoptosis in Cerebral Ischemia/Reperfusion Injury".CNS NEUROSCIENCE & THERAPEUTICS 19.8(2013):566-576.
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