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The atypical chemokine receptor 3 interacts with Connexin 43 inhibiting astrocytic gap junctional intercellular communication

Author

Listed:
  • Amos Fumagalli

    (Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM)

  • Joyce Heuninck

    (Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM)

  • Anne Pizzoccaro

    (Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM)

  • Enora Moutin

    (Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM)

  • Joyce Koenen

    (Université Paris-Saclay, Inserm, Inflammation, Microbiome and Immunosurveillance
    Amsterdam Institute for Molecules Medicines and Systems, Division of Medicinal Chemistry, Faculty of Sciences, VU University Amsterdam)

  • Martial Séveno

    (Biocampus Montpellier, Université de Montpellier, CNRS, INSERM)

  • Thierry Durroux

    (Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM)

  • Marie-Pierre Junier

    (CNRS UMR8246, Inserm U1130, Neuroscience Paris Seine-IBPS, Sorbonne Universités)

  • Géraldine Schlecht-Louf

    (Université Paris-Saclay, Inserm, Inflammation, Microbiome and Immunosurveillance)

  • Francoise Bachelerie

    (Université Paris-Saclay, Inserm, Inflammation, Microbiome and Immunosurveillance)

  • Dagmar Schütz

    (Institute of Pharmacology and Toxicology, Jena University Hospital)

  • Ralf Stumm

    (Institute of Pharmacology and Toxicology, Jena University Hospital)

  • Martine J. Smit

    (Amsterdam Institute for Molecules Medicines and Systems, Division of Medicinal Chemistry, Faculty of Sciences, VU University Amsterdam)

  • Nathalie C. Guérineau

    (Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM)

  • Séverine Chaumont-Dubel

    (Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM)

  • Philippe Marin

    (Institut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM)

Abstract

The atypical chemokine receptor 3 (ACKR3) plays a pivotal role in directing the migration of various cellular populations and its over-expression in tumors promotes cell proliferation and invasiveness. The intracellular signaling pathways transducing ACKR3-dependent effects remain poorly characterized, an issue we addressed by identifying the interactome of ACKR3. Here, we report that recombinant ACKR3 expressed in HEK293T cells recruits the gap junction protein Connexin 43 (Cx43). Cx43 and ACKR3 are co-expressed in mouse brain astrocytes and human glioblastoma cells and form a complex in embryonic mouse brain. Functional in vitro studies show enhanced ACKR3 interaction with Cx43 upon ACKR3 agonist stimulation. Furthermore, ACKR3 activation promotes β-arrestin2- and dynamin-dependent Cx43 internalization to inhibit gap junctional intercellular communication in primary astrocytes. These results demonstrate a functional link between ACKR3 and gap junctions that might be of pathophysiological relevance.

Suggested Citation

  • Amos Fumagalli & Joyce Heuninck & Anne Pizzoccaro & Enora Moutin & Joyce Koenen & Martial Séveno & Thierry Durroux & Marie-Pierre Junier & Géraldine Schlecht-Louf & Francoise Bachelerie & Dagmar Schüt, 2020. "The atypical chemokine receptor 3 interacts with Connexin 43 inhibiting astrocytic gap junctional intercellular communication," Nature Communications, Nature, vol. 11(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-18634-y
    DOI: 10.1038/s41467-020-18634-y
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