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2021-10-06 - Article/Dans un journal avec peer-review - Anglais - 13 page(s)

Lantoine Joséphine, Proces Anthony , Villers Agnès , Halliez Sophie, Buée Luc, Ris Laurence , Gabriele Sylvain , "Inflammatory Molecules Released by Mechanically Injured Astrocytes Trigger Presynaptic Loss in Cortical Neuronal Networks" in ACS Chemical Neurosciences

  • Edition : American Chemical Society (DC)
  • Codes CREF : Neurophysiologie (DI3224), Biologie moléculaire (DI3111), Neuropathologie (DI332C), Biophysique (DI3113), Biomécanique (DI3118), Biologie cellulaire (DI311D)
  • Unités de recherche UMONS : Laboratoire Interfaces et Fluides complexes (S885), Neurosciences (M119)
  • Instituts UMONS : Institut des Biosciences (Biosciences)
Texte intégral :

Abstract(s) :

(Anglais) Deformation, compression, or stretching of brain tissues cause diffuse axonal injury (DAI) and induce structural and functional alterations of astrocytes, the most abundant cell type in the brain. To gain further insight into the role of mechanically activated astrocytes on neuronal networks, this study was designed to investigate whether cytokines released by mechanically activated astrocytes can affect the growth and synaptic connections of cortical neuronal networks. Astrocytes were cultivated on elastic membranes and subjected to repetitive mechanical insults, whereas well-defined protein micropatterns were used to form standardized neuronal networks. GFAP staining showed that astrocytes were mechanically activated after two cycles of stretch and mesoscale discovery assays indicated that injured astrocytes released four major cytokines. To understand the role of these cytokines, neuronal networks were cultured with the supernatant of healthy or mechanically activated astrocytes, and the individual contribution of the proinflammatory cytokine tumor necrosis factor-α (TNF-α) was studied. We found that the supernatant of two-cycle stretched astrocytes decreased presynaptic terminals and indicated that TNF-α must be considered a key player of the synaptic loss. Furthermore, our results indicate that cytokines released by injured astrocytes significantly modulate the balance between TNFR1 and TNFR2 receptors by enhancing R2 receptors. We demonstrated that TNF-α is not involved in this process, suggesting a predominant role of other secreted cytokines. Together, these results contribute to a better understanding of the consequences of repetitive astrocyte deformations and highlight the role of inflammatory signaling pathways in synaptic plasticity and modulation of TNFR1 and TNFR2 receptors.

Notes :
  • (Anglais) Joséphine Lantoine and Anthony Procès contributed equally to this work.
Identifiants :
  • PMID : 34614352
  • DOI : 10.1021/acschemneuro.1c00488f

Mots-clés :
  • (Anglais) Cytokines
  • (Anglais) Neuronal Network
  • (Anglais) Astrocytes
  • (Anglais) Mechanical Injury