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ATP-mediated cytotoxicity in microglial cells

D Ferrari1, P Chiozzi, S Falzoni

  • 1Institute of General Pathology, University of Ferrara, Italy.

Neuropharmacology
|November 19, 1997
PubMed

Insights

Microglial cells expressing the P2Z/P2X7 receptor are sensitive to ATP-mediated cell death. This study identifies the P2Z/P2X7 receptor

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Microglial cells, the immune cells of the central nervous system, express purinergic receptors for extracellular ATP.
  • Both P2Y and P2X receptor subtypes are known to be present, with a particular focus on the pore-forming P2Z/P2X7 receptor.

Purpose of the Study:

  • To identify and characterize the P2Z/P2X7 receptor in microglial cells (N9 and N13 cell lines).
  • To investigate the role of the P2Z/P2X7 receptor in ATP-mediated cytotoxicity in microglial cells.
  • To explore the mechanism of ATP-mediated cell death and ATP release in activated microglial cells.

Main Methods:

  • Utilized a specific polyclonal antibody to identify the P2Z/P2X7 receptor in N9 and N13 microglial cell lines.
  • Assessed ATP-mediated cytotoxicity in microglial cells with and without P2Z/P2X7 receptor expression.
  • Transfected HEK293 cells with P2X7 receptor cDNA to confirm its role in cytotoxicity.
  • Performed morphological and biochemical analyses to determine the mode of cell death.

Main Results:

  • Confirmed the presence of the P2Z/P2X7 receptor in N9 and N13 microglial cells.
  • Microglial cells expressing P2Z/P2X7 were highly sensitive to ATP-induced cell death, while resistant clones lacked the receptor.
  • HEK293 cells transfected with P2X7 cDNA became susceptible to ATP cytotoxicity.
  • ATP-dependent cell death in microglial cells was identified as apoptosis.
  • Activated microglial cells released ATP via a non-lytic mechanism.

Conclusions:

  • The P2Z/P2X7 receptor plays a critical role in mediating ATP-induced apoptosis in microglial cells.
  • Microglial cells can release ATP through a non-lytic pathway upon activation by bacterial endotoxin.
  • These findings suggest a purinergic autocrine/paracrine signaling loop in microglial activation and cell death.

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