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000169804 0247_ $$2doi$$a10.1016/j.freeradbiomed.2021.07.001
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000169804 0247_ $$2ISSN$$a0891-5849
000169804 0247_ $$2ISSN$$a1873-4596
000169804 037__ $$aDKFZ-2021-01558
000169804 041__ $$aEnglish
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000169804 1001_ $$aGamara, Jouda$$b0
000169804 245__ $$aArf6 regulates energy metabolism in neutrophils.
000169804 260__ $$aNew York, NY [u.a.]$$bElsevier$$c2021
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000169804 520__ $$aThe small GTPase Arf6 regulates many cellular processes, including cytoskeletal remodeling, receptor endocytosis, and pathogen phagocytosis. Arf6 silencing in neutrophil (PMN)-like cells is well-known to inhibit chemotactic peptide-mediated activation of phospholipase D, the oxidative burst, and β2 integrin-dependent adhesion. In conditional knockout (cKO) mice, the migration to inflammatory sites of Arf6-deficient PMNs was diminished and associated with reduced cell surface expression of β2 integrins. In this study we assessed the impact of Arf6 depletion on the functions and gene expression profile of PMNs isolated from the mouse air pouch. Numerous genes involved in response to oxygen levels, erythrocyte and myeloid differentiation, macrophage chemotaxis, response to chemicals, apoptosis, RNA destabilization, endosome organization, and vesicle transport were differentially expressed in PMNs cKO for Arf6. Lpar6 and Lacc-1 were the most up-regulated and down-regulated genes, respectively. The deletion of Arf6 also decreased Lacc-1 protein level in PMNs, and silencing of Arf6 in THP-1 monocytic cells delayed LPS-mediated Lacc-1 expression. We report that fMLP or zymosan-induced glycolysis and oxygen consumption rate were both decreased in air pouch PMNs but not in bone marrow PMNs of Arf6 cKO mice. Reduced oxygen consumption correlated with a decrease in superoxide and ROS production. Deletion of Arf6 in PMNs also reduced phagocytosis and interfered with apoptosis. The data suggest that Arf6 regulates energy metabolism, which may contribute to impaired phagocytosis, ROS production, and apoptosis in PMN-Arf6 cKO. This study provides new information on the functions and the inflammatory pathways influenced by Arf6 in PMNs.
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000169804 650_7 $$2Other$$aApoptosis
000169804 650_7 $$2Other$$aArf6
000169804 650_7 $$2Other$$aConditional knockout
000169804 650_7 $$2Other$$aFAMIN
000169804 650_7 $$2Other$$aGlycolysis
000169804 650_7 $$2Other$$aInflammation
000169804 650_7 $$2Other$$aMetabolism
000169804 650_7 $$2Other$$aMouse
000169804 650_7 $$2Other$$aNeutrophil
000169804 650_7 $$2Other$$aPhagocytosis
000169804 650_7 $$2Other$$aROS
000169804 650_7 $$2Other$$aSuperoxide
000169804 7001_ $$aDavis, Lynn$$b1
000169804 7001_ $$aLeong, Andrew Z$$b2
000169804 7001_ $$aPagé, Nathalie$$b3
000169804 7001_ $$aRollet-Labelle, Emmanuelle$$b4
000169804 7001_ $$aZhao, Chenqi$$b5
000169804 7001_ $$0P:(DE-He78)876d213ee6559a5e98ddf2113698ed0b$$aHongu, Tsunaki$$b6$$udkfz
000169804 7001_ $$aFunakoshi, Yuji$$b7
000169804 7001_ $$aKanaho, Yasunori$$b8
000169804 7001_ $$aAoudji, Fawzi$$b9
000169804 7001_ $$aPelletier, Martin$$b10
000169804 7001_ $$aBourgoin, Sylvain G$$b11
000169804 773__ $$0PERI:(DE-600)1483653-1$$a10.1016/j.freeradbiomed.2021.07.001$$gVol. 172, p. 550 - 561$$p550 - 561$$tFree radical biology and medicine$$v172$$x0891-5849$$y2021
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