Endoplasmic Reticulum Is a Key Organella in Bradykinin-Triggered ATP Release From Cultured Smooth Muscle Cells
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- Zhao Yumei
- Department of Pharmacology, School of Medicine, Fukuoka University, Japan Department of Pedodontics, School of Dentistry of Shanghai Tongji University, China
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- Migita Keisuke
- Rehabilitation Medicine, Institute Brain Science, Hirosaki University School of Medicine, Japan
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- Sato Chiemi
- Department of Pharmacology, School of Medicine, Fukuoka University, Japan
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- Usune Sadaharu
- Research Laboratory of Biodynamics, School of Medicine, Fukuoka University, Japan
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- Iwamoto Takahiro
- Department of Pharmacology, School of Medicine, Fukuoka University, Japan
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- Katsuragi Takeshi
- Department of Pharmacology, School of Medicine, Fukuoka University, Japan Medical Research Center, School of Medicine, Fukuoka University, Japan
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ATP has broad functions as an autocrine/paracrine molecule. The mode of ATP release and its intracellular source, however, are little understood. Here we show that bradykinin via B2-receptor stimulation induces the extracellular release of ATP via the inositol 1,4,5-trisphosphate [Ins(1,4,5)P3]-signaling pathway in cultured taenia coli smooth muscle cells. It was found that bradykinin also increased the production of Ins(1,4,5)P3 and 2-APB-inhibitable [Ca2+]i. The evoked release of ATP was suppressed by the Ca2+-channel blockers, nifedipine, and verapamil. Moreover, the extracellular release of ATP was elicited by photoliberation of Ins(1,4,5)P3. Bradykinin caused a quick and transient accumulation of intracellular ATP from cells treated with 1% perchloric acid solution (PCA), but not with the cell lysis buffer. Peak accumulation was prevented by 2-APB and thapsigargin, but not by nifedipine or verapamil, inhibitors of extracellular release of ATP. These findings suggest that bradykinin elicits the extracellular release of ATP that is mediated by the Ins(1,4,5)P3-induced Ca2+ signaling and, finally, leads to a Ca2+-dependent export of ATP from the cells. Furthermore, the bradykinin-induced transient accumulation of ATP in the cells treated with PCA may imply a possible release of ATP from the endoplasmic reticulum.<br>
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 105 (1), 57-65, 2007
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680155039616
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- NII論文ID
- 10024315703
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 8918810
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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
- NDL
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