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首页> 外文期刊>American Journal of Physiology >Aldosterone responsiveness of A6 cells is restored by cloned rat mineralocorticoid receptor (see comments)
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Aldosterone responsiveness of A6 cells is restored by cloned rat mineralocorticoid receptor (see comments)

机译：克隆的大鼠盐皮质激素受体可恢复A6细胞的醛固酮反应性（参见评论）

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摘要

A6 cells, derived from Xenopus laevis renal tubule, form a high-resistance ion-transporting monolayer when grown on permeable supports and can generate a short-circuit current (SCC) that is stimulated by high levels of the mineralocorticoid aldosterone. Surprisingly, A6 SCC is more responsive to glucocorticoids than to mineralocorticoids, suggesting the possibility that these cells do not contain transcriptionally active mineralocorticoid receptor (MR) and that glucocorticoid receptor (GR) mediates MR-like responses in these collecting duct-like cells. We have examined the response of both SCC and a transfected reporter gene to mineralocorticoids and glucocorticoids in the presence and absence of transfected rat MR (rMR). We found that, in the absence of transfected MR, a reporter gene that can be activated by MR or GR was more responsive to glucocorticoids such as dexamethasone and RU-28362 than to mineralocorticoids such as aldosterone. Transfected rMR underwent mineralocorticoid-dependent nuclear localization and restored both transcriptional sensitivity of a reporter gene and SCC response to mineralocorticoids. These data demonstrate that A6 cells contain transcriptionally active GR but not MR and thus suggest a molecular basis for the defect in A6 cell SCC response to aldosterone. Our results also demonstrate that GR is capable of mediating hormone stimulation of SCC, a classic mineralocorticoid response. Finally, the observation that heterologous expression of rMR can localize normally to the A6 nucleus in a hormone-dependent fashion and restore both the transcriptional and SCC response to mineralocorticoids suggests that MR function is conserved in species as distantly related as toads and mammals.
机译：源自非洲爪蟾肾脏肾小管的A6细胞在可渗透性支持物上生长时会形成高电阻的离子传输单层，并且会产生由高水平的盐皮质激素醛固酮刺激的短路电流（SCC）。出乎意料的是，A6 SCC对糖皮质激素的反应性比对盐皮质激素的反应性高，这提示这些细胞不含转录活性盐皮质激素受体（MR），而糖皮质激素受体（GR）介导了这些收集导管样细胞中的MR样反应。我们已经检查了存在和不存在转染大鼠MR（rMR）的情况下，SCC和转染的报告基因对盐皮质激素和糖皮质激素的反应。我们发现，在没有转染的MR的情况下，可以被MR或GR激活的报告基因对糖皮质激素（如地塞米松和RU-28362）的反应性要比对盐皮质激素（如醛固酮）的反应高。转染的rMR经历了盐皮质激素依赖性核定位，并恢复了报告基因的转录敏感性和对盐皮质激素的SCC反应。这些数据表明，A6细胞包含转录活性GR，但不包含MR，因此提示A6细胞SCC对醛固酮的反应存在缺陷的分子基础。我们的结果还表明，GR能够介导SCC的激素刺激，这是经典的盐皮质激素反应。最后，关于rMR异源表达可以激素依赖性方式正常定位于A6核并恢复对盐皮质激素的转录和SCC反应的观察结果表明，MR功能在与蟾蜍和哺乳动物密切相关的物种中得以保留。

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