TRPM4 Channels Mediate Hypertonicity-induced, Ca²⁺-impermeable, Non-selective Cation Currents in a Cervical Cancer Cell Line, HeLa Cells
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- GOMI Simmon
- Department of Molecular Pharmacology, Shinshu University School of Medicine Department of Cardiovascular Medicine, Shinshu University School of Medicine
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- NAKADA Tsutomu
- Department of Molecular Pharmacology, Shinshu University School of Medicine
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- KASHIHARA Toshihide
- Department of Molecular Pharmacology, Shinshu University School of Medicine
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- IKEDA Uichi
- Department of Cardiovascular Medicine, Shinshu University School of Medicine
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- YAMADA Mitsuhiko
- Department of Molecular Pharmacology, Shinshu University School of Medicine
書誌事項
- タイトル別名
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- TRPM4 Channels Mediate Hypertonicity-induced, Ca<sup>2+</sup>-impermeable, Non-selective Cation Currents in a Cervical Cancer Cell Line, HeLa Cells
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抄録
When extracellular osmolarity exceeds intracellular osmolarity, cells initially shrink but then approach the original cell volume by so-called regulatory cell volume increase (RVI). RVI operates under physiological conditions so that impairment of RVI leads to immediate cell cycle arrest and apoptosis. In a cervical cancer cell line, HeLa cells, extracellular hypertonicity induced non-selective cation currents (IHO currents) which transported mainly Na+ into cells to induce RVI as assessed with the patch-clamp method. Ion channels mediating these currents were Ca2+-impermeable and sensitive to flufenamic acid (FFA) and econazole but not to amiloride or ruthenium red. RT-PCR indicated that HeLa cells express transient receptor potential (TRP) C1, C6, M3, M4, M7, M8, V1 and V2 subunits which form non-selective cation channels. From these results, we speculated that TRPM4 may mediate IHO currents. Indeed, transduction of a dominant-negative TRPM4 subunit significantly inhibited IHO currents. TRPM4 channels became insensitive to hypertonic stimulus when intracellular Ca2+ was strongly buffered. Thus, extracellular hypertonicity activates TRPM4 channels through intracellular Ca2+ to induce RVI in HeLa cells. These results indicate that intra-uterus or -vaginal application of drugs blocking TRPM4 channels may cause antiproliferative/proapoptotic effects on cervical cancer.
収録刊行物
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- 信州医学雑誌
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信州医学雑誌 62 (1), 33-44, 2014
信州医学会
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詳細情報 詳細情報について
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- CRID
- 1390001204211726336
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- NII論文ID
- 130004551913
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- NII書誌ID
- AN00120815
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- ISSN
- 18846580
- 00373826
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- HANDLE
- 10091/17380
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- NDL書誌ID
- 025277140
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- IRDB
- NDL
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可