Cytosolic Ca2+ alteration mediates both ryanodine receptor and IP3 receptor in TE671/RD cells

DOI IR 16 References
  • EDAHIRO Shigeki
    Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science
  • YOSHIKAWA Hiroaki
    Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science Health Service Center Kanazawa University
  • IWASA Kazuo
    Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science
  • HASHII Minako
    Department of Biophysical Genetics, Kanazawa University Graduate School of Medical Science
  • YAMADA Masahito
    Department of Neurology and Neurobiology of Aging, Kanazawa University Graduate School of Medical Science

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Abstract

TE671/RD is a cell line obtained from the rhabdomyosarcoma cells. In the present study, we examined [Ca2+]i alteration induced by acetylcholine (ACh) in TE671/RD cells with the special attention to ryanodine receptor (RyR) and inositol 1, 4, 5-trisphosphate receptor (IP3R). The change of [Ca2+]i was mediated by muscarinic type 3 (m3) AChR. Both phosphatidylinositol-specific phospholipase C blocker (U73122) and IP3R blocker (2-APB) inhibited ACh-induced [Ca2+]i elevation, suggesting that IP3 pathway is involved in [Ca2+]i alteration. Ryanodine and FK506 increased ACh-induced [Ca2+]i elevation, which was decreased by RyR blocker (ruthenium red). These results suggest that RyR and FK506 binding protein 12 kDa (FKBP12) complex was involved in [Ca2+]i change, and that TE671/RD cell line has a hybrid characteristic of smooth and skeletal muscles.

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