Prostaglandin E<sub>2</sub>-Induced Cell Death is Mediated by Activation of EP2 Receptors in Motor Neuron-like NSC-34 Cells

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  • Miyagishi Hiroko
    Laboratory of Pharmacology, School of Pharmacy, Nihon University, Japan
  • Kosuge Yasuhiro
    Laboratory of Pharmacology, School of Pharmacy, Nihon University, Japan
  • Yoneoka Yuki
    Laboratory of Pharmacology, School of Pharmacy, Nihon University, Japan
  • Ozone Maiko
    Laboratory of Pharmacology, School of Pharmacy, Nihon University, Japan
  • Endo Manami
    Laboratory of Pharmacology, School of Pharmacy, Nihon University, Japan
  • Osada Nobuhiro
    Laboratory of Pharmacology, School of Pharmacy, Nihon University, Japan
  • Ishige Kumiko
    Laboratory of Pharmacology, School of Pharmacy, Nihon University, Japan
  • Kusama-Eguchi Kuniko
    Laboratory of Biochemistry, School of Pharmacy, Nihon University, Japan
  • Ito Yoshihisa
    Laboratory of Pharmacology, School of Pharmacy, Nihon University, Japan

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  • Prostaglandin E₂-Induced Cell Death is Mediated by Activation of EP2 Receptors in Motor Neuron-like NSC-34 Cells

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Abstract

Prostaglandin E2 (PGE2) was shown to induce neuronal death in the CNS. To characterize the neurotoxicity of PGE2 and E-prostanoid receptors (EP) in motor neurons, we investigated PGE2-induced cell death and the type(s) of EP responsible for mediating it in NSC-34, a motor neuron-like cell line. Immunoblotting studies showed that EP2 and EP3 were dominantly expressed in NSC-34 cells and motor neurons in mice. Exposure to PGE2 and butaprost, an EP2 agonist, but not sulprostone, an EP1/3 agonist, resulted in decreased viability of these cells. These results suggest that PGE2 induces cell death by activation of EP2 in NSC-34 cells.

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