https://scholars.lib.ntu.edu.tw/handle/123456789/137702
標題: | Lysophospholipids Attenuate Acetylcholine-evoked Ca2+ Responses in Bovine Chromaffin Cells 水解磷酸脂抑制牛嗜鉻細胞被乙醯膽鹼刺激所引起的鈣離子反應 |
作者: | Li-Long Lu Chien-Yuan Pan |
關鍵字: | Ca2+ channel;G-protein-coupled receptor;lysophosphatidic acid;muscarinic receptor;nicotinic receptor;sphingosine 1-phosphate;鈣離子通道;G蛋白連結受器;水解磷酸脂;蕈毒鹼受器;尼古丁受器;鞘胺醇 1-磷酸鹽 | 公開日期: | 三月-2010 | 卷: | 55 | 期: | 1 | 起(迄)頁: | 060-066 | 來源出版物: | Taiwania | 摘要: | 交感神經節前神經分泌乙醯膽鹼,刺激腎上腺嗜鉻細胞將兒茶酚胺釋放到血液中,以反應短期壓力。乙醯膽鹼活化尼古丁及蕈毒鹼受器,提高胞內鈣離子濃度([Ca(上标 2+)]i)因而釋放兒茶酚胺。而在血液中,由免疫細胞所分泌的水解磷酸脂(lysophospholipids, LPLs),包括鞘胺醇1-磷酸鹽(sphingosine 1-phosphate, S1P)及溶血磷脂酸(lysophosphatidic acid, LPA),則會引起許多不同的生理反應。為探討LPLs對嗜鉻細胞[Ca(上标 2+)]i變化的效應,細胞先以鈣離子指示劑Fura-2標定,以觀察[Ca(上标 2+)]i的變化。再以1μMS1P或LPA處理0、10、20、30、40、50、或60分鐘後,以乙醯膽鹼(100μM)、蕈毒鹼(100μM)、DMPP(10μM)、或高鉀溶液(50mM KCl)刺激5秒。結果顯示在LPA或S1P處理20分鐘後,乙醯膽鹼所引起的[Ca(上标 2+)]i上升,受到明顯的抑制。然而高鉀溶液所引起的[Ca(上标 2+)]i上升,並不會受到S1P前處理的影響,但會被LPA所增加。蕈毒鹼刺激所引起的反應,僅會受LPLs稍微抑制;然而以DMPP活化尼苦丁受器所引起的[Ca(上标 2+)]i反應,則會受到LPA及S1P的顯著抑制。這些結果顯示,LPLs可能主要是透過抑制尼古丁受器,而達到抑制乙醯膽鹼所引起的[Ca(上标 2+)]i上升。 Adrenal medulla chromaffin cells are stimulated by acetylcholine released from sympathetic preganglionic neurons and secret catecholamines into the blood to accommodate short-term stress. Acetylcholine activates nicotinic and muscarinic receptors to elevate the intracellular Ca2+ concentration and causes the secretion of catecholamines. Lysophospholipids in the serum, including sphingosine 1-phosphate (S1P) and lysophosphatidic acid (LPA), are released primarily from immune cells during blood clotting and infection to modulate various physiological activities. To characterize the effects of lysophospholipids on Ca2+ responses in bovine chromaffin cells, cells were loaded with the Ca2+ indicator fura-2, and fluorescence intensity was used to monitor changes in intracellular Ca2+ concentration. Cells treated with 1 μM S1P or LPA for 0, 10, 20, 30, 40, 50, or 60 min were stimulated with acetylcholine (100 μM), muscarine (100 μM), DMPP (10 μM), or high K+ buffer (50 mM KCl) for 5 sec. The results showed that the Ca2+ responses evoked by acetylcholine were significantly inhibited after incubation in LPA or S1P for 20 min. The Ca2+ response evoked by high K+ buffer was not inhibited by S1P pretreatment and was significantly facilitated by LPA pretreatment. Muscarine-evoked Ca2+ responses were slightly attenuated by LPA and S1P pretreatments. Nicotine-evoked responses were inhibited in both LPA- and S1P-pretreated cells. Our findings demonstrate that nicotinic receptors may be the main targets of lysophospholipids in inhibiting acetylcholine-evoked Ca2+ responses. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/283383 http://ntur.lib.ntu.edu.tw/bitstream/246246/283383/1/5501_201003_9.pdf |
顯示於: | 生命科學系 |
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5501_201003_9.pdf | 4.1 MB | Adobe PDF | 檢視/開啟 |
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