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	Mitochondrial proteomic analysis and characterization of the intracellular mechanisms of bis(7)-tacrine in protecting against glutamate-induced excitotoxicity in primary cultured neurons
	Fu, Hongjun ; Li, Wenming ; Liu, Yulin ; Lao, Yuanzhi ; Liu, Wei ; Chen, Cheng ; Yu, Hua ; Lee, Nelson T. K. ; Chang, Donald C. ; Li, Peng ; Pang, Yuanping ; Tsim, Karl W. K. ; Li, Mingtao ; Han, Yifan
	2010-05-11 ; 2010-05-11
关键词	bis(7)-tacrine glutamate mitochondria cerebellar granule neurons two-dimensional differential in-gel electrophoresis MALDI-TOF/MS ANTI-ALZHEIMERS AGENT ALDEHYDE DEHYDROGENASE INCREASES NITRIC-OXIDE SYNTHASE D-ASPARTATE RECEPTORS GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE ACETYLCHOLINESTERASE INHIBITOR OXIDATIVE-PHOSPHORYLATION PERMEABILITY TRANSITION GEL-ELECTROPHORESIS INDUCED APOPTOSIS Biochemical Research Methods
中文摘要	Increasing evidence supports that the mitochondrial dysfunction, mainly caused by abnormal changes in mitochondrial proteins, plays a pivotal role in glutamate-induced excitotoxicity, which is closely associated with the pathogenesis of acute and chronic neurodegenerative disorders, such as stroke and Alzheimer's disease. In this study, post-treatment of cerebellar granule neurons with bis(7)-tacrine significantly reversed declines in mitochondrial membrane potential, ATP production, and neuronal cell death induced by glutamate. Moreover, this reversal was independent of NMDA antagonism, acetylcholinesterase inhibition, and cholinergic pathways. Using two-dimensional differential in-gel electrophoresis, we conducted a comparative analysis of mitochondrial protein patterns. In all, 29 proteins exhibiting significant differences in their abundances were identified in the glutamate-treated group when compared with the control. The expression patterns in 22 out of these proteins could be reversed by post-treatment with bis(7)-tacrine. Most of the differentially expressed proteins are involved in energy metabolism, oxidative stress, and apoptosis. In particular, the altered patterns of four of these proteins were further validated by Western blot analysis. Our findings suggest that multiple signaling pathways initiated by the altered mitochondrial proteins may mediate glutamate-induced excitotoxicity and also offer potentially useful intracellular targets for the neuroprotection provided by bis(7)-tacrine.
语种	英语 ; 英语
出版者	AMER CHEMICAL SOC ; WASHINGTON ; 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
内容类型	期刊论文
源URL	[http://hdl.handle.net/123456789/26947]
专题	清华大学
推荐引用方式 GB/T 7714	Fu, Hongjun,Li, Wenming,Liu, Yulin,et al. Mitochondrial proteomic analysis and characterization of the intracellular mechanisms of bis(7)-tacrine in protecting against glutamate-induced excitotoxicity in primary cultured neurons[J],2010, 2010.
APA	Fu, Hongjun.,Li, Wenming.,Liu, Yulin.,Lao, Yuanzhi.,Liu, Wei.,...&Han, Yifan.(2010).Mitochondrial proteomic analysis and characterization of the intracellular mechanisms of bis(7)-tacrine in protecting against glutamate-induced excitotoxicity in primary cultured neurons..
MLA	Fu, Hongjun,et al."Mitochondrial proteomic analysis and characterization of the intracellular mechanisms of bis(7)-tacrine in protecting against glutamate-induced excitotoxicity in primary cultured neurons".(2010).

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