Maitotoxin stimulates Cd influx in Madin-Darby kidney cells by activating Ca-permeable cation channels.
Maitotoxin stimulates Cd influx in Madin-Darby kidney cells by activating Ca-permeable cation channels.
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DOI：
10.1054/ceca.1999.0115
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发表时间：
2000-04
期刊：
影响因子：
4
通讯作者：
L. Olivi;J. Bressler
中科院分区：
文献类型：
--
作者：
L. Olivi;J. Bressler
本研究探讨了钙通道在 Madin-Darby 犬肾 (MDCK) 细胞摄取镉 (Cd) 过程中的作用。 Maitotoxin 是不同类型钙通道的激活剂，可增加 MDCK 细胞中 109Cd 和 45Ca 的积累。我们发现麦芽毒素通过刺激 109Cd 流入来增加积累，因为它不影响流出。钙池操纵的 Ca 通道抑制剂 SKF96365 部分阻断 45Ca 流入，但不影响 109Cd 流入。 Ni 和 Mn、洛哌丁胺和 proadifen (SKF 525a) 可抑制麦毒毒素刺激的细胞中 45Ca 和 109Cd 的流入，但 La 和硝苯地平则不然。用佛波醇 12, 13-异丁酸酯 (PDBu) 过夜处理以激活蛋白激酶 C，导致刺激 45Ca 和 109Cd 流入所需的麦芽毒素浓度降低。用蛋白激酶 C 抑制剂 GF109203X 处理细胞可阻断 PDBu 的作用。此外，在用 RNA 合成放线菌素 D 抑制剂处理的细胞中，PDBu 的作用消失。这些结果表明，与电压依赖性和钙库操作的 Ca 通道不同，Ca 渗透性阳离子通道介导 MDCK 细胞中 Cd 的摄取。该通道的表达受蛋白激酶 C 调节。
This study examined the role of calcium channels for the uptake of cadmium (Cd) into Madin-Darby canine kidney (MDCK) cells. Maitotoxin, an activator of different types of calcium channels, increased accumulation of 109Cd and 45Ca in MDCK cells. We found that maitotoxin increased accumulation by stimulating 109Cd influx because it did not affect efflux. An inhibitor of store-operated Ca channels, SKF96365, partially blocked 45Ca influx but did not affect 109Cd influx. Ni and Mn, and loperamide and proadifen (SKF 525a), inhibited 45Ca and 109Cd influx in cells stimulated with maitotoxin, but La and nifedipine did not. Overnight treatment with phorbol 12, 13-ibutyrate (PDBu) to activate protein kinase C resulted in a decrease in the concentration of maitotoxin needed to stimulate 45Ca and 109Cd influx. The effect of PDBu was blocked by treating cells with the protein kinase C inhibitor GF109203X. Additionally, the effect of PDBu was lost in cells treated with an inhibitor of RNA synthesis actinomycin D. These results suggest that a Ca permeable cation channel different from voltage-dependent and store-operated Ca channels mediates the uptake of Cd in MDCK cells. The expression of this channel is regulated by protein kinase C.