Microscopic heat pulse-induced calcium dynamics in single WI-38 fibroblasts.
Microscopic heat pulse-induced calcium dynamics in single WI-38 fibroblasts.
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DOI：
10.2142/biophysics.10.109
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Ishiwata S
中科院分区：
文献类型：
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作者：
Itoh H;Oyama K;Suzuki M;Ishiwata S
温度敏感的Ca 2+动力学主要通过瞬时受体电位通道发生，但也通过内质网膜上的Ca 2+通道和泵发生。因此，细胞质Ca 2+浓度（[Ca 2 +]cyt）通过环境温度的变化重新平衡。本研究探讨了热脉冲（加热持续时间：2 s或150 s）对单个WI-38成纤维细胞（被视为正常细胞）胞浆内[Ca 2 +]的影响。我们发现，Ca 2+爆发后立即发生短（2秒）的热脉冲，这是我们以前的报告对HeLa细胞相似，但具有较低的热敏性。在光学显微镜下，将源自聚焦的1455 nm红外激光的热脉冲施加在细胞附近。用肌质/内质网Ca ~（2+）ATP酶抑制剂（SERCA）或三磷酸肌醇受体（IP 3R）处理细胞，可抑制热脉冲诱导的Ca ~（2+）爆发。长（150秒）的热脉冲也诱导Ca 2+爆发后，开始加热，并立即重新冷却。细胞在生理温度（37°C）下比在室温（25°C）下更热敏感;然而，在37°C下，细胞在更高温度（环境温度+热脉冲）下响应。这些结果强烈表明，热脉冲诱导的Ca 2+爆发是由瞬时的不平衡，在Ca 2+流之间的SERCA和IP 3R，并提供了一个潜在的新方法热控制Ca 2+调节的细胞功能。
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.