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Title of Journal: J Bioenerg Biomembr

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Abbravation: Journal of Bioenergetics and Biomembranes

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Springer US

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DOI

10.1007/s11120-005-9009-9

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1573-6881

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Inhibitory effect of homocysteine on rat neural st

Authors: XuMei Zhang YaQian Zhao Hai Yan Huan Liu GuoWei Huang
Publish Date: 2016/12/02
Volume: 49, Issue: 2, Pages: 131-138
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Abstract

Increased blood plasma concentration of the sulphur amino acid homocysteine Hcy is considered as an independent risk factor of the neurodegenerative diseases However the detailed molecular mechanisms by which Hcy leads to neurotoxicity have yet to be clarified Recent research has suggested that neurotoxicity of Hcy may involve negative regulation of neural stem cell NSC proliferation In the current study primary NSCs were isolated from neonatal rat brain hippocampus and the inhibition in cell growth was observed after exposure to l50 μM and 500 μM LHcy The changes in protein expression were monitored with densitometric 2D–gel electrophoresis coupled with MALDITOF mass spectrometry Proteomic analysis revealed that the expression levels of two mitochondrial proteins cytochrome bc1 complex2 UQCRC2 the major component of electron transport chain complex III and aconitase an enzyme involved in the tricarboxylic acid cycle were decreased in Hcy treatment group compared to control group Protein expression was further verified by Western blot and their enzymatic activities were also downregulated in NSCs after Hcy treatment Restoration of aconitase and UQCRC2 protein levels using their expression vectors could partly rescue the cell viability inhibition caused by Hcy Moreover Hcy caused the increase in the intracellular levels of reactive oxygen species ROS and the decrease in ATP content which are known to play important roles in the cellular stress response of the cell growth Altogether the results suggest that the decreased expression and enzymatic activities of the mitochondrial proteins may be possible causes of the overproduction of ROS and depletion of ATP The inhibition in cell growth at the end of Hcy treatment was probably due to the changes in protein expression and mitochondrial dysfunction in vitro cultures of NSCs

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