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<p>Aquaporin-4 (AQP4), the main astrocytic water channel, assembles into supramolecular structures known as Orthogonal Arrays of Particles (OAPs). While AQP4-mediated water fluxes are known to influence cytoskeletal dynamics at the single-cell level, their role in collective migration remain unclear. Using primary WT and OAP-deficient (OAP-null) astrocytes, we investigated cell migration under control and proinflammatory conditions. In wound healing assays, control OAP-null astrocytes exhibited greater migratory capacity, while inflamed cells were largely immotile. Particle Image Velocimetry revealed genotype and condition-specific migration patterns, with OAP-null astrocytes displaying more linear trajectories. Cytokine treatment also reduced AQP4 and Connexin-43 expression and impaired gap-junctional communication in both genotypes. Calcein-AM quenching assays showed reduced water permeability in OAP-null cells, independently of treatment. These findings highlight the supramolecular organization of AQP4 as a key determinant of astrocyte collective migration and suggest that chronic inflammation induces a poorly coordinated phenotype through dysregulation of AQP4 and gap-junctional networks.</p>

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Supramolecular aggregation of aquaporin-4 shapes astrocyte collective migration and mechanics

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月22日

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  • Barbara Barile,
  • Nicholas John Mennona,
  • Maria Grazia Mola,
  • Alessia Memeo,
  • Antonio Cibelli,
  • Roberto Barbaro,
  • Matilde Colella,
  • Antonio Frigeri,
  • Valentina Benfenati,
  • Wolfgang Losert,
  • Grazia Paola Nicchia

摘要

Aquaporin-4 (AQP4), the main astrocytic water channel, assembles into supramolecular structures known as Orthogonal Arrays of Particles (OAPs). While AQP4-mediated water fluxes are known to influence cytoskeletal dynamics at the single-cell level, their role in collective migration remain unclear. Using primary WT and OAP-deficient (OAP-null) astrocytes, we investigated cell migration under control and proinflammatory conditions. In wound healing assays, control OAP-null astrocytes exhibited greater migratory capacity, while inflamed cells were largely immotile. Particle Image Velocimetry revealed genotype and condition-specific migration patterns, with OAP-null astrocytes displaying more linear trajectories. Cytokine treatment also reduced AQP4 and Connexin-43 expression and impaired gap-junctional communication in both genotypes. Calcein-AM quenching assays showed reduced water permeability in OAP-null cells, independently of treatment. These findings highlight the supramolecular organization of AQP4 as a key determinant of astrocyte collective migration and suggest that chronic inflammation induces a poorly coordinated phenotype through dysregulation of AQP4 and gap-junctional networks.