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Regulation of superoxide production in neutrophils: role of calcium influx
Author(s) -
Bréchard Sabrina,
Tschirhart Eric J.
Publication year - 2008
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0807553
Subject(s) - nadph oxidase , superoxide , microbiology and biotechnology , calcium , extracellular , calcium signaling , reactive oxygen species , intracellular , biology , calcium in biology , stimulation , oxidative stress , respiratory burst , oxidase test , biochemistry , chemistry , enzyme , endocrinology , organic chemistry
Upon stimulation, activation of NADPH oxidase complexes in neutrophils produces a burst of superoxide anions contributing to oxidative stress and the development of inflammatory process. Store‐operated calcium entry (SOCE), whereby the depletion of intracellular stores induces extracellular calcium influx, is known to be a crucial element of NADPH oxidase regulation. However, the mechanistic basis mediating SOCE is still only partially understood, as is the signal‐coupling pathway leading to modulation of store‐operated channels. This review emphasizes the role of calcium influx in the control of the NADPH oxidase and summarizes the current knowledge of pathways mediating this extracellular calcium entry in neutrophils. Such investigations into the cross‐talk between NADPH oxidase and calcium might allow the identification of novel pharmacological targets with clinical use, particularly in inflammatory diseases.