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Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Oxid+Med+Cell+Longev 2016 ; 2016 (ä): ä Nephropedia Template TP
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Intermittent Hypoxia Affects the Spontaneous Differentiation In Vitro of Human Neutrophils into Long-Lived Giant Phagocytes #MMPMID26635914
Dyugovskaya L; Berger S; Polyakov A; Lavie P; Lavie L
Oxid Med Cell Longev 2016[]; 2016 (ä): ä PMID26635914show ga
Previously we identified, for the first time, a new small-size subset of neutrophil-derived giant phagocytes (G?) which spontaneously develop in vitro without additional growth factors or cytokines. G? are CD66b+/CD63+/MPO+/LC3B+ and are characterized by extended lifespan, large phagolysosomes, active phagocytosis, and reactive oxygen species (ROS) production, and autophagy largely controls their formation. Hypoxia, and particularly hypoxia/reoxygenation, is a prominent feature of many pathological processes. Herein we investigated G? formation by applying various hypoxic conditions. Chronic intermittent hypoxia (IH) (29 cycles/day for 5 days) completely abolished G? formation, while acute IH had dose-dependent effects. Exposure to 24?h (56 IH cycles) decreased their size, yield, phagocytic ability, autophagy, mitophagy, and gp91-phox/p22-phox expression, whereas under 24?h sustained hypoxia (SH) the size and expression of LC3B and gp91-phox/p22-phox resembled G? formed in normoxia. Diphenyl iodide (DPI), a NADPH oxidase inhibitor, as well as the PI3K/Akt and autophagy inhibitor LY294002 abolished G? formation at all oxygen conditions. However, the potent antioxidant, N-acetylcysteine (NAC) abrogated the effects of IH by inducing large CD66b+/LC3B+ G? and increased both NADPH oxidase expression and phagocytosis. These findings suggest that NADPH oxidase, autophagy, and the PI3K/Akt pathway are involved in G? development.