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Mechanisms underlying extracellular ATP-evoked interleukin-6 release in mouse microglial cell line, MG-5

Y Shigemoto-Mogami1, S Koizumi, M Tsuda

  • 1Division of Pharmacology, National Institute of Health Sciences, Setagaya, Tokyo, Japan.

Insights

Adenosine triphosphate (ATP) triggers interleukin-6 (IL-6) release from microglia via P2Y receptors, activating p38 and protein kinase C (PKC). This reveals a new pathway for cytokine induction in the central nervous system (CNS).

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Microglia are key immune cells in the central nervous system (CNS).
  • Microglia synthesize cytokines, crucial signaling molecules.
  • Interleukin-6 (IL-6) is an important cytokine with diverse roles.

Purpose of the Study:

  • To investigate the mechanisms of ATP-evoked IL-6 production in microglia.
  • To identify the specific receptors and signaling pathways involved in IL-6 induction.

Main Methods:

  • Utilized a mouse microglial cell line (MG-5).
  • Examined the effects of ATP and its analogs on IL-6 production.
  • Assessed the activation of mitogen-activated protein kinases (MAPKs) and protein kinase C (PKC).
  • Investigated the roles of P2X7 and P2Y receptors using specific agonists and inhibitors.

Main Results:

  • ATP induced IL-6 production in a concentration-dependent manner.
  • Activation of p38 MAPK, but not ERK, was involved in IL-6 induction.
  • P2Y receptors, not P2X7 receptors, were primarily responsible for ATP-evoked IL-6 release.
  • Inhibition of Ca(2+)-dependent PKC attenuated IL-6 production.
  • The identified P2Y receptor was pertussis toxin (PTX)-insensitive and linked to phospholipase C.

Conclusions:

  • ATP activates PTX-insensitive P2Y receptors on microglia.
  • This activation leads to p38 MAPK and Ca(2+)-dependent PKC activation.
  • A novel signaling pathway involving P2Y receptors, p38, and PKC mediates IL-6 mRNA expression and release in microglia.

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