Glucocorticoids regulate NHE-3 transcription in OKP cells
Glucocorticoids regulate NHE-3 transcription in OKP cells
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DOI：
10.1152/ajprenal.1996.270.1.f164
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发表时间：
1996-01-01
期刊：
影响因子：
--
通讯作者：
Moe, OW
中科院分区：
文献类型：
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作者：
Baum, M;Amemiya, M;Moe, OW
KP细胞表达NHE-3，这是一种抗氨酰胺的Na+/H+反转运蛋白，可能是近端小管分泌根尖质子的异构体。我们之前的研究表明，OKP细胞中耐阿米洛利钠离子/氢离子反转运蛋白受地塞米松（一种合成糖皮质激素）的调节。本研究的目的是探讨糖皮质激素介导的Na+/H+反转运蛋白活性增加的机制。用10(-6)M地塞米松孵育OKP细胞导致NHE-3 mRNA丰度增加2至3倍。用地塞米松孵育4小时后观察到这种增加，时间过程与Na+/ h +反转运蛋白活性相似。为了研究NHE-3 mRNA丰度增加的机制，我们进行了mRNA半衰期和体外转录实验。在对照组和地塞米松处理的细胞中，NHE-3 mRNA的半衰期为8 h。用地塞米松处理OKP细胞时，体外转录率提高1.8倍。这些数据表明糖皮质激素介导的Na+/H+反转运蛋白活性的增加是由于NHE-3基因转录的增加。
KP cells express NHE-3, an amiloride-resistant Na+/H+ antiporter, which is likely an isoform responsible for apical proton secretion by the proximal tubule. We have previously shown that an amiloride-resistant Na+/H+ antiporter in OKP cells is regulated by dexamethasone, a synthetic glucocorticoid. The purpose of the present study was to examine the mechanism for the glucocorticoid-mediated increase in Na+/H+ antiporter activity. Incubation of OKP cells with 10(-6) M dexamethasone resulted in a two- to threefold increase in NHE-3 mRNA abundance. This increase was seen after 4 h of incubation with dexamethasone, a time course similar to that found for Na+/H+ antiporter activity. To examine the mechanism for the increase in NHE-3 mRNA abundance, mRNA half-life and in vitro transcription experiments were performed. NHE-3 mRNA had a half-life of 8 h in control and dexamethasone-treated cells. The rate of in vitro transcription was 1.8-fold greater when OKP cells were treated with dexamethasone. These data suggest that the glucocorticoid-mediated increase in Na+/H+ antiporter activity is due to an increase in NHE-3 gene transcription.