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首页> 外文期刊>Life sciences >Mechanism of lanthanum inhibition of extracellular ATP-evoked calcium mobilization in MDCK cells.
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Mechanism of lanthanum inhibition of extracellular ATP-evoked calcium mobilization in MDCK cells.

机译：镧抑制MDCK细胞中胞外ATP引起的钙动员的机制。

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摘要

We have studied the effects of La3+ on ATP-evoked rises in intracellular calcium levels ([Ca2+]i) measured by fura-2 fluorimetry in Madin Darby canine kidney (MDCK) cells. ATP evoked [Ca2+]i rises dose-dependently with an EC50 of 2.5 microM. The trigger for the Ca2+ signal was a release of Ca2+ from the inositol-1,4,5-trisphosphate (IP3)-sensitive stores because the signal was completely blocked by pretreatment with the endoplasmic reticulum (ER) Ca2+ pump inhibitor thapsigargin (TG) or the phospholipase C (PLC) inhibitor U73122. Both the peak height and area under the curve of 10 microM ATP-evoked Ca2+ signal was reduced by approximately 50% by extracellular Ca2+ removal, suggesting that ATP induced capacitative Ca2+ entry. La3+ inhibited the ATP-evoked Ca2+ signal dose-dependently when added before or after ATP. Pretreatment of 0.1 mM La3+ inhibited approximately 90% of the Ca2+ signal induced by 10 microM ATP. The mechanisms underlying the La3+ inhibition appear to involve not only block of capacitative Ca2+ entry but also interference with ATP binding to the ATP receptors.
机译：我们已经研究了呋喃2荧光法测定的Mad3 Darby犬肾（MDCK）细胞中La3 +对ATP引起的细胞内钙水平（[Ca2 +] i）升高的影响。 ATP诱发的[Ca2 +] i剂量依赖性增加，EC50为2.5 microM。 Ca2 +信号的触发因素是从肌醇-1,4,5-三磷酸（IP3）敏感的存储区释放了Ca2 +，因为该信号已被内质网（ER）预处理Ca2 +泵抑制剂thapsigargin（TG）完全阻断了或磷脂酶C（PLC）抑制剂U73122。通过去除细胞外Ca2 +，将10 microM ATP诱发的Ca2 +信号的峰高和曲线下面积都降低了约50％，这表明ATP诱导了电容性Ca2 +进入。当在ATP之前或之后添加La3 +时，剂量依赖性地抑制ATP诱发的Ca2 +信号。 0.1 mM La3 +的预处理抑制了10 microM ATP诱导的Ca2 +信号的大约90％。 La3 +抑制的潜在机制似乎不仅涉及阻断Ca2 +的进入，而且还干扰ATP与ATP受体的结合。

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