| Literature DB >> 27597056 |
D V Grigorieva1, I V Gorudko1, A V Sokolov2,3, V A Kostevich2,3, V B Vasilyev2, S N Cherenkevich1, O M Panasenko4.
Abstract
Myeloperoxidase, heme enzyme of azurophilic granules in neutrophils, is released into the extracellular space in the inflammation foci. In neutrophils, it stimulates a dose-dependent release of lactoferrin (a protein of specific granules), lysozyme (a protein of specific and azurophilic granules), and elastase (a protein of azurophilic granules). 4-Aminobenzoic acid hydrazide, a potent inhibitor of peroxidase activity of myeloperoxidase, produced no effect on neutrophil degranulation. Using signal transduction inhibitors (genistein, methoxyverapamil, wortmannin, and NiCl2), we demonstrated that myeloperoxidase-induced degranulation of neutrophils resulted from enzyme interaction with the plasma membrane and depends on activation of tyrosine kinases, phosphatidylinositol 3-kinases (PI3K), and calcium signaling. Myeloperoxidase modified by oxidative/halogenation stress (chlorinated and monomeric forms of the enzyme) lost the potency to activate neutrophil degranulation.Entities:
Keywords: human neutrophils; myeloperoxidase; neutrophil degranulation; oxidative/halogenation stress; signaling systems
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Year: 2016 PMID: 27597056 DOI: 10.1007/s10517-016-3446-7
Source DB: PubMed Journal: Bull Exp Biol Med ISSN: 0007-4888 Impact factor: 0.804