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Related Experiment Videos

p38/SAPK2 controls gap junction closure in astrocytes.

Darina Zvalova1, Jocelyne Cordier, Marc Mesnil

  • 1Chaire de Neuropharmacologie, INSERM U114, Collège de France, Paris, France.

Glia
|March 30, 2004
PubMed
Summary

p38/stress-activated protein kinase 2 (p38/SAPK2) mediates the inhibition of astrocyte gap junction communication (GJC) induced by interleukin-1beta and sorbitol. This pathway involves protein kinase C (PKC) and impacts central nervous system injury signaling.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Astrocyte gap junction communication (GJC) is implicated in propagating death signals after central nervous system (CNS) injury.
  • Inhibition of p38/stress-activated protein kinase 2 (p38/SAPK2) has shown promise in reducing lesion size after cerebral ischemia.

Purpose of the Study:

  • To investigate the role of p38/SAPK2 in modulating astrocyte GJC.
  • To explore the involvement of interleukin-1beta (IL-1beta) and hyperosmolarity-induced p38/SAPK2 activation in GJC inhibition.

Main Methods:

  • Primary mouse astrocyte cultures were treated with IL-1beta and sorbitol.
  • Dye coupling assays were used to measure GJC.
  • p38/SAPK2 activation and translocation were assessed via immunocytochemistry.

Related Experiment Videos

  • Pharmacological inhibitors (SB203580, PKC inhibitors) were employed.

    • Main Results:

    • Both IL-1beta and sorbitol rapidly inhibited GJC and activated/translocated p38/SAPK2.
    • The p38/SAPK2 inhibitor SB203580 blocked these effects and reversed GJC inhibition.
    • Sorbiol-induced GJC inhibition involved increased phosphorylation of protein kinase C (PKC) substrates, which was blocked by SB203580 and PKC inhibitors.
    • Connexin 43 expression and phosphorylation remained unchanged.

    Conclusions:

    • p38/SAPK2 is a central mediator of IL-1beta and sorbitol-induced inhibition of astrocyte GJC.
    • Protein kinase C (PKC) acts as a downstream effector of p38/SAPK2 in this signaling pathway.
    • These findings highlight a novel mechanism regulating GJC relevant to CNS injury.