期刊
FEBS LETTERS
卷 584, 期 10, 页码 2076-2084出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2010.02.073
关键词
Intracellular chloride channel 1; Microglia; Reactive oxygen species; Nicotinamide adenine dinucleotide phosphate oxidase; Alzheimer disease; Charge compensation
资金
- MRC [G0601943] Funding Source: UKRI
- Medical Research Council [G0601943] Funding Source: researchfish
- Medical Research Council [G0601943] Funding Source: Medline
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.
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