Chloride intracellular channel 1 (CLIC1): Sensor and effector during oxidative stress

被引:97
作者
Averaimo, Stefania [1 ]
Milton, Rosemary H. [2 ]
Duchen, Michael R. [2 ]
Mazzanti, Michele [1 ]
机构
[1] Univ Milan, Dipartimento Sci Biomol & Biotecnol, I-20133 Milan, Italy
[2] UCL, Dept Cell & Dev Biol, London WC1E 6BT, England
基金
英国医学研究理事会;
关键词
Intracellular chloride channel 1; Microglia; Reactive oxygen species; Nicotinamide adenine dinucleotide phosphate oxidase; Alzheimer disease; Charge compensation; MICROGLIAL NADPH OXIDASE; GATED PROTON CHANNELS; ION-CHANNEL; ALZHEIMERS-DISEASE; HUMAN-NEUTROPHILS; A-BETA; GLUTATHIONE TRANSFERASE; CELL-CYCLE; PROTEIN; NCC27;
D O I
10.1016/j.febslet.2010.02.073
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Oxidative stress, characterized by overproduction of reactive oxygen species (ROS), is a major feature of several pathological states. Indeed, many cancers and neurodegenerative diseases are accompanied by altered redox balance, which results from dysregulation of nicotinamide adenine dinucleotide phosphate ( NADPH) oxidase. In this review, we consider the role of the intracellular chloride channel 1 (CLIC1) in microglial cells during oxidative stress. Following microglial activation, CLIC1 translocates from the cytosol to the plasma membrane where it promotes a chloride conductance. The resultant anionic current balances the excess charge extruded by the active NADPH oxidase, supporting the generation of superoxide by the enzyme. In this scenario, CLIC1 could be considered to act as both a second messenger and an executor. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:2076 / 2084
页数:9
相关论文
共 57 条
[1]   Characterisation of electron currents generated by the human neutrophil NADPH oxidase [J].
Ahluwalia, Jatinder .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2008, 368 (03) :656-661
[2]   Chloride channels activated by swell can regulate the NADPH oxidase generated membrane depolarisation in activated human neutrophils [J].
Ahluwalia, Jatinder .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2008, 365 (02) :328-333
[3]   The NOX family of ROS-generating NADPH oxidases: Physiology and pathophysiology [J].
Bedard, Karen ;
Krause, Karl-Heinz .
PHYSIOLOGICAL REVIEWS, 2007, 87 (01) :245-313
[4]  
Behrend L, 2003, BIOCHEM SOC T, V31, P1441
[5]   Microglia-mediated neurotoxicity: uncovering the molecular mechanisms [J].
Block, Michelle L. ;
Zecca, Luigi ;
Hong, Jau-Shyong .
NATURE REVIEWS NEUROSCIENCE, 2007, 8 (01) :57-69
[6]  
Boillée S, 2008, J CLIN INVEST, V118, P474, DOI [10.1172/JC134613, 10.1172/JCI34613]
[7]   Maternal smoking-A contributor to the obesity epidemic? [J].
Chen, Hui ;
Morris, Margaret J. .
OBESITY RESEARCH & CLINICAL PRACTICE, 2007, 1 (03) :155-163
[8]   From glutathione transferase to pore in a CLIC [J].
Cromer, BA ;
Morton, CJ ;
Board, PG ;
Parker, MW .
EUROPEAN BIOPHYSICS JOURNAL WITH BIOPHYSICS LETTERS, 2002, 31 (05) :356-364
[9]   Oligomeric and fibrillar species of amyloid-β peptides differentially affect neuronal viability [J].
Dahlgren, KN ;
Manelli, AM ;
Stine, WB ;
Baker, LK ;
Krafft, GA ;
LaDu, MJ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (35) :32046-32053
[10]   Charge compensation for NADPH oxidase activity in microglia in rat brain slices does not involve a proton current [J].
De Simoni, Anna ;
Allen, Nicola J. ;
Attwell, David .
EUROPEAN JOURNAL OF NEUROSCIENCE, 2008, 28 (06) :1146-1156