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Reticulon 4A/Nogo-A influences the distribution of Kir4.1 but is not essential for potassium conductance in retinal Müller glia.
Journal article

Reticulon 4A/Nogo-A influences the distribution of Kir4.1 but is not essential for potassium conductance in retinal Müller glia.

  • Joly S CUO-Recherche, Médecine Régénératrice-Centre de recherche FRQS du CHU de Québec-Université Laval, Université Laval, Québec, Canada; Centre de Recherche en Organogénèse expérimentale de l'Université Laval/LOEX, Québec, QC, Canada; Département d'Ophtalmologie, Faculté de médecine, Université Laval, Québec, QC, Canada.
  • Dodd DA University of Texas Southwestern Medical Center, Department of Microbiology, Dallas, TX, USA.
  • Grewe BF Institute of Neuroinformatics, ETH Zurich, Zurich, Switzerland.
  • Pernet V CUO-Recherche, Médecine Régénératrice-Centre de recherche FRQS du CHU de Québec-Université Laval, Université Laval, Québec, Canada; Centre de Recherche en Organogénèse expérimentale de l'Université Laval/LOEX, Québec, QC, Canada; Département d'Ophtalmologie, Faculté de médecine, Université Laval, Québec, QC, Canada. Electronic address: vincent.pernet.1@ulaval.ca.
  • 2016-06-09
Published in:
  • Neuroscience letters. - 2016
Glia
Kir4.1
Müller cells
Nogo-A
Retina
Adenoviridae
Animals
Aquaporin 4
Cells, Cultured
Dystrophin
Ependymoglial Cells
Genetic Vectors
Male
Mice
Mice, Inbred C57BL
Nogo Proteins
Potassium
Potassium Channels, Inwardly Rectifying
Rats
Up-Regulation
English In the adult retina, we have previously shown that Nogo-A was highly expressed in Müller glia. However, the role of Nogo-A in the glial cell physiology is not clear. In this study, we investigated the possible influence that Nogo-A may exert on other polarized molecules in Müller cells, in particular inwardly rectifying potassium channel 4.1 (Kir4.1) and aquaporin 4 (AQP4) that respectively control potassium and water exchange in glial cells. Our results showed that adenovirus-mediated Nogo-A overexpression with AdNogo-A increased the immunofluorescent signal of Kir4.1 in rat Müller cell line 1 (rMC-1) cells but did not change its expression level by Western blotting. In vivo, AdNogo-A induced ectopic Kir4.1 immunoreactivity throughout the radial processes of Müller cells compared with AdLacZ control virus. Surprisingly, AdNogo-A did not modify the distribution of Dp71 and AQP4 that are common binding partners for Kir4.1 in the dystrophin-associated protein (DAP) complex anchored at the plasma membrane of Müller glia. Immunoprecipitation experiments revealed molecular interactions between Nogo-A and Kir4.1. In Nogo-A KO mouse retinae, the distribution of Kir4.1 was not different from that observed in Wild-Type (WT) animals. In addition, potassium conductance did not change in freshly dissociated Nogo-A KO Müller glia compared with WT cells. In summary, the increase of Nogo-A expression can selectively influence the distribution of Kir4.1 in glia but is not essential for Kir4.1-mediated potassium conductance at the plasma membrane in physiological conditions. Nogo-A-Kir4.1 interactions may, however, contribute to pathological processes taking place in the retina, for instance, after ischemia.
Language
  • English
Open access status
closed
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Persistent URL
https://sonar.ch/global/documents/223354
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