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A Glycine Site-Specific NMDA Receptor Antagonist Protects Retina Ganglion Cells From Ischemic Injury by Modulating Apoptotic Cascades
Qiu, Weiqiang1; Wei, Ruoxin1; Zhang, Chi1; Zhang, Chun1; Leng, Wen2; Wang, Wei1
刊名JOURNAL OF CELLULAR PHYSIOLOGY
2010-06-01
DOI10.1002/jcp.22118
223期:3页:819-826
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cell Biology ; Physiology
研究领域[WOS]Cell Biology ; Physiology
关键词[WOS]AMINO-ACID NEUROTOXICITY ; NITRIC-OXIDE SYNTHASE ; REPERFUSION INJURY ; TRANSIENT ISCHEMIA ; NEURONAL DEATH ; UP-REGULATION ; CYTOCHROME-C ; RAT RETINA ; GLUTAMATE ; FAMILY
英文摘要

Glutamate neurotoxicity is one of the causative factors leading to neural degeneration including retina. Inhibition of NMDA receptors has been shown neuroprotective effects. However, specifically inhibition of glycine subunit in NMDA receptors and its effects on retina neural protection has not been tested. In this study, using a glycine site-specific NMDA receptor antagonist, we investigated its neuroprotective effects on rat retinal ganglion cells (RGCs) from a transient ischemic injury and its possible underlying mechanisms. Following an ischemia/reperfusion injury the structural damages of rat retinas were assessed by an immunofluorescence method and the apoptosis of retinal neural cells was evaluated by using a terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) method. The survived RGCs were labeled by retrograde manner and counted on whole-mounted retinas. In the presence of glycine site-specific NMDA receptor antagonist, the thickness of retina was sustained, especially in the inner nuclear layers compared with mock controls. While a significantly higher numbers of TUNEL-positive apoptotic cells and fewer of RGCs were observed in the retina without the glycine antagonist, indicating its strong protective roles. Some apoptotic factors such as Bax, Bcl-2, CAMK II, COX I, COX4, Caspase-3, and GRINI gene have been tested from retinal samples with or without the glycine antagonist. A significantly lower of expressions of Bax, CAMK II, COX I, COX4, Caspase-3, and GRIN I have been shown in the retinas with the antagonist. Bcl-2/Bax ratio was significantly higher with the antagonist, suggested that the glycine site-specific NMDA receptor antagonist protecting RGC death might through inhibition of apoptotic signaling. J. Cell. Physiol. 223: 819-826, 2010. (C) 2010 Wiley-Liss, Inc.

语种英语
WOS记录号WOS:000277482900031
引用统计
被引频次:9[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/400002259/67924
专题北京大学第三临床医学院_眼科
作者单位1.Beijing Guang An Nat Healthcare Inst, Beijing, Peoples R China
2.Peking Univ, Hosp 3, Dept Ophthalmol, Beijing 100191, Peoples R China
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GB/T 7714
Qiu, Weiqiang,Wei, Ruoxin,Zhang, Chi,et al. A Glycine Site-Specific NMDA Receptor Antagonist Protects Retina Ganglion Cells From Ischemic Injury by Modulating Apoptotic Cascades[J]. JOURNAL OF CELLULAR PHYSIOLOGY,2010,223(3):819-826.
APA Qiu, Weiqiang,Wei, Ruoxin,Zhang, Chi,Zhang, Chun,Leng, Wen,&Wang, Wei.(2010).A Glycine Site-Specific NMDA Receptor Antagonist Protects Retina Ganglion Cells From Ischemic Injury by Modulating Apoptotic Cascades.JOURNAL OF CELLULAR PHYSIOLOGY,223(3),819-826.
MLA Qiu, Weiqiang,et al."A Glycine Site-Specific NMDA Receptor Antagonist Protects Retina Ganglion Cells From Ischemic Injury by Modulating Apoptotic Cascades".JOURNAL OF CELLULAR PHYSIOLOGY 223.3(2010):819-826.
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