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首页> 外文期刊>Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research >Depolarization of osteoclast plasma membrane potential by 17beta-estradiol.
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Depolarization of osteoclast plasma membrane potential by 17beta-estradiol.

机译：17β-雌二醇使破骨细胞质膜电位去极化。

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摘要

The effect of estrogen on plasma membrane potential of isolated avian osteoclasts was examined through the use of a fluorescent potential-sensitive dye, bis-(1,3-dibutylbarbiturate) trimethine oxonol, also known as bis-oxonol. A decrease in potential was observed within seconds of addition of 17beta-estradiol. Ouabain, a specific Na+K+-ATPase inhibitor, and BaCl2, an inhibitor of the inwardly rectifying K+ channel, blocked the estrogen response. Verapamil and lanthanum chloride (LaCl3), inhibitors of inward Ca2+ channels, and 4'4-diisothiocyanatostilbene-2'2-disulfonic acid (DIDS), an inhibitor of Cl- channels, did not affect the depolarization. Herbimycin A, a tyrosine kinase inhibitor, also had no effect on the decreased membrane potential. These data provide evidence which suggests that estrogen regulates osteoclasts through ion channel activities. The change in K+ channel activity was observed within seconds of addition of 17beta-estradiol, indicating an action at the level of the plasma membrane.
机译：通过使用荧光电位敏感染料bis-（1,3-dibutylbarbiturate）trimethine oxonol，也称为bis-oxonol，检查了雌激素对分离的禽破骨细胞质膜电位的影响。在添加17β-雌二醇的几秒钟内观察到电位降低。瓦巴因（一种特殊的Na + K + -ATPase抑制剂）和BaCl2（一种向内整流的K +通道的抑制剂）阻断了雌激素的反应。维拉帕米和氯化镧（LaCl3），是内向Ca2 +通道的抑制剂，而4'4-二异硫氰酸根合-2烯2'2-二磺酸（DIDS），是Cl-通道的抑制剂，不影响去极化作用。酪氨酸激酶抑制剂除草霉素A对降低的膜电位也没有影响。这些数据提供了表明雌激素通过离子通道活性调节破骨细胞的证据。在添加17β-雌二醇的几秒钟内观察到K +通道活性的变化，表明在质膜水平上有作用。

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