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@ARTICLE{Gamara:169804,
      author       = {J. Gamara and L. Davis and A. Z. Leong and N. Pagé and E.
                      Rollet-Labelle and C. Zhao and T. Hongu$^*$ and Y. Funakoshi
                      and Y. Kanaho and F. Aoudji and M. Pelletier and S. G.
                      Bourgoin},
      title        = {{A}rf6 regulates energy metabolism in neutrophils.},
      journal      = {Free radical biology and medicine},
      volume       = {172},
      issn         = {0891-5849},
      address      = {New York, NY [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2021-01558},
      pages        = {550 - 561},
      year         = {2021},
      abstract     = {The 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.},
      subtyp        = {Review Article},
      keywords     = {Apoptosis (Other) / Arf6 (Other) / Conditional knockout
                      (Other) / FAMIN (Other) / Glycolysis (Other) / Inflammation
                      (Other) / Metabolism (Other) / Mouse (Other) / Neutrophil
                      (Other) / Phagocytosis (Other) / ROS (Other) / Superoxide
                      (Other)},
      cin          = {A014},
      ddc          = {610},
      cid          = {I:(DE-He78)A014-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34245858},
      doi          = {10.1016/j.freeradbiomed.2021.07.001},
      url          = {https://inrepo02.dkfz.de/record/169804},
}