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Adenosine A2A receptors regulate oxidative stress formation in rat pheochromocytoma PC12 cells during serum

Nai-Kuei Huang1

  • 1National Research Institute of Chinese Medicine, No. 155-1, Li-Nung Street, Sec. 2, Ship-Pai, Peitou, Taipei 112, Taiwan, ROC. andrew@mail.nricm.edu.tw

Neuroscience Letters
|September 16, 2003
PubMed

Insights

Activation of adenosine A2A receptors (A2A-Rs) protects PC12 cells from oxidative stress and apoptosis via a protein kinase A (PKA) pathway. This mechanism involves reducing reactive oxygen species (ROS) formation.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Serum deprivation induces oxidative stress and apoptosis in PC12 cells.
  • Adenosine A2A receptors (A2A-Rs) are implicated in cellular protection.
  • Reactive oxygen species (ROS) play a key role in cellular damage and death.

Purpose of the Study:

  • To investigate the role of A2A-R activation in preventing apoptosis and ROS formation in serum-deprived PC12 cells.
  • To elucidate the signaling pathway, specifically the involvement of protein kinase A (PKA), in A2A-R-mediated protection.
  • To determine if A2A-R activation can protect against other forms of oxidative stress, such as H2O2-induced cell death.

Main Methods:

  • Utilized pheochromocytoma PC12 cell line.
  • Applied serum deprivation and H2O2 treatment to induce cellular stress.
  • Administered A2A-R agonists, PKA inhibitors, PKA stimulators, antioxidants, and antioxidative system-interrupting agents.
  • Assessed cell viability, apoptosis, and ROS formation.

Main Results:

  • A2A-R activation prevented ROS formation and apoptosis in serum-deprived PC12 cells.
  • A PKA inhibitor blocked the anti-apoptotic effects of A2A-R and reversed ROS suppression, indicating a PKA-dependent pathway.
  • PKA stimulators and antioxidants mimicked the protective effects of A2A-R activation against serum-deprived ROS formation and apoptosis.
  • A2A-R activation protected against H2O2-induced cell death.
  • Agents that interrupted the antioxidative system attenuated A2A-R-mediated protection.

Conclusions:

  • A2A-R activation confers protection against serum deprivation-induced apoptosis in PC12 cells.
  • The protective mechanism involves PKA-dependent regulation and attenuation of oxidative stress.
  • A2A-Rs may represent a therapeutic target for conditions involving oxidative stress and neuronal cell death.

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