Serum-dependence of AMPA receptor-mediated proliferation in glioma cells

DOI
  • Yoshida Yukari
    Dept. Neurophysiol., Gunma Univ. Grad. Sch. Med., Maebashi, Gunma, Japan
  • Tsuzuki Keisuke
    Dept. Neurophysiol., Gunma Univ. Grad. Sch. Med., Maebashi, Gunma, Japan
  • Ishiuchi Shogo
    Dept. Neurosurg., Gunma Univ. Grad. Sch. Med., Maebashi, Gunma, Japan
  • Ozawa Seiji
    Dept. Neurophysiol., Gunma Univ. Grad. Sch. Med., Maebashi, Gunma, Japan

Bibliographic Information

Other Title
  • グリオーマ細胞におけるAMPA受容体を介した細胞増殖の血清依存性

Abstract

Glutamate may cause Ca2+ entry through Ca2+-permeable glutamate receptors, which in turn stimulates the anti-apoptotic signaling cascade in glioma cells. Here, we found that a human glioma cell line, U-87 MG, expressed GluR1, GluR2 and GluR3 subunits of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate acid-type glutamate receptors (AMPARs). Approximately 20% of GluR2 was expressed in the unedited form, which is known to assemble Ca2+-permeable AMPARs. Ca2+ entry through the activation of these receptors by AMPA was detected clearly in approximately 20% of U-87 MG glioma cells. Cell proliferation assays revealed that the application of AMPA or glutamate facilitated cell proliferation by activating AMPARs in low-serum medium containing 0.5% fetal calf serum (FCS). Unexpectedly, cell proliferation by the activation of AMPARs was not detected in serum-rich medium containing 10% FCS. Overexpression of the unedited form of GluR2 (GluR2Q) by adenoviral-mediated gene transfer markedly increased the Ca2+ entry into U-87 MG cells. This treatment in the presence of glutamate facilitated proliferation and migration of U-87 MG cells in the low-serum condition, whereas it had again no effect in the serum-rich condition. It is therefore likely that cell proliferation and migration of U-87 MG cells are under the regulation of growth factors contained in the serum as well as Ca2+ entry through AMPARs, and that the latter regulation becomes evident only when serum factors are deprived of culture medium. [J Physiol Sci. 2006;56 Suppl:S117]

Journal

Details 詳細情報について

  • CRID
    1390282680705186176
  • NII Article ID
    130005448278
  • DOI
    10.14849/psjproc.2006.0_117_4
  • Data Source
    • JaLC
    • CiNii Articles
  • Abstract License Flag
    Disallowed

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