Microscopic heat pulse-induced calcium dynamics in single WI-38 fibroblasts
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- Itoh Hideki
- Department of Pure and Applied Physics, Graduate School of Advanced Science and Engineering, Waseda University Institute of Medical Biology, Agency for Science Technology & Research (A*STAR)
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- Oyama Kotaro
- Department of Physics, Faculty of Advanced Science and Engineering, Waseda University
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- Suzuki Madoka
- Waseda Bioscience Research Institute in Singapore (WABIOS) Organization for University Research Initiatives, Waseda University
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- Ishiwata Shin’ichi
- Department of Pure and Applied Physics, Graduate School of Advanced Science and Engineering, Waseda University Department of Physics, Faculty of Advanced Science and Engineering, Waseda University Waseda Bioscience Research Institute in Singapore (WABIOS) Organization for University Research Initiatives, Waseda University
抄録
Temperature-sensitive Ca2+ dynamics occur primarily through transient receptor potential channels, but also by means of Ca2+ channels and pumps on the endoplasmic reticulum membrane. As such, cytoplasmic Ca2+ concentration ([Ca2+]cyt) is re-equilibrated by changes in ambient temperature. The present study investigated the effects of heat pulses (heating duration: 2 s or 150 s) on [Ca2+]cyt in single WI-38 fibroblasts, which are considered as normal cells. We found that Ca2+ burst occurred immediately after short (2 s) heat pulse, which is similar to our previous report on HeLa cells, but with less thermosensitivity. The heat pulses originated from a focused 1455-nm infrared laser light were applied in the vicinity of cells under the optical microscope. Ca2+ bursts induced by the heat pulse were suppressed by treating cells with inhibitors for sarco/endoplasmic reticulum Ca2+ ATPase (SERCA) or inositol trisphosphate receptor (IP3R). Long (150 s) heat pulses also induced Ca2+ bursts after the onset of heating and immediately after re-cooling. Cells were more thermosensitive at physiological (37°C) than at room (25°C) temperature; however, at 37°C, cells were responsive at a higher temperature (ambient temperature+heat pulse). These results strongly suggest that the heat pulse-induced Ca2+ burst is caused by a transient imbalance in Ca2+ flow between SERCA and IP3R, and offer a potential new method for thermally controlling Ca2+-regulated cellular functions.
収録刊行物
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- BIOPHYSICS
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BIOPHYSICS 10 (0), 109-119, 2014
日本生物物理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680197922176
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- NII論文ID
- 130004940803
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- ISSN
- 13492942
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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
- Crossref
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- 抄録ライセンスフラグ
- 使用不可