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A(2A) adenosine receptor ligands and proinflammatory cytokines induce PC 12 cell death through apoptosis

Maria L Trincavelli1, Alessandra Falleni, Beatrice Chelli

  • 1Dipartimento di Psichiatria, Neurobiologia, Farmacologia e Biotecnologie, University of Pisa, Via Bonanno 6, 56126 Pisa, Italy.

Biochemical Pharmacology
|November 6, 2003
PubMed

Insights

Proinflammatory cytokines and A(2A) adenosine receptor agonists induce PC 12 cell death via apoptosis. A(2A) adenosine receptors regulate cell survival and death in response to inflammatory mediators.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cell Biology

Background:

  • A(2A) adenosine receptor signaling is crucial in the central nervous system, implicated in both physiological functions and pathological conditions.
  • This receptor is a potential therapeutic target for various nervous system diseases.

Purpose of the Study:

  • To investigate cell death induction in PC 12 cells treated with proinflammatory cytokines and adenosine receptor ligands.
  • To identify the specific adenosine receptor subtypes involved in cytokine- and adenosine-mediated cytotoxicity.

Main Methods:

  • PC 12 cells were treated with Interleukin-1-beta (IL-1-beta), tumor necrosis factor-alpha (TNF-alpha), and various adenosine receptor agonists and antagonists.
  • Cell viability was assessed, and specific receptor involvement was determined using selective agonists/antagonists.
  • Apoptosis was confirmed using ELISA and transmission electron microscopy (TEM).

Main Results:

  • IL-1-beta, TNF-alpha, and a non-selective adenosine receptor agonist (NECA) significantly reduced PC 12 cell viability.
  • Selective A(2A) adenosine receptor agonists reduced cell viability, an effect blocked by an A(2A) antagonist (SCH58261) but not an A(2B) antagonist (MRS1706).
  • Cytokines and A(2A) receptor ligands induced cell death through apoptosis.

Conclusions:

  • A(2A) adenosine receptors play a significant role in controlling PC 12 cell survival and death.
  • These receptors modulate cellular responses to tissue damage and inflammatory mediator production.
  • Findings highlight the A(2A) adenosine receptor as a key mediator in inflammatory processes affecting neuronal cells.

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