糖皮质激素调节的基因amiloride-sensitive半规管导管上皮钠转运途径的新生儿老鼠。

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邓Pondugula SR Raveendran NN, Ergonul Z, Y,陈J, Sanneman JD,帕默LG,马库斯

糖皮质激素调节的基因amiloride-sensitive半规管导管上皮钠转运途径的新生儿老鼠。

基因组学杂志,2006年1月12日,24(2):114 - 23所示。Epub 2005年11月1日。

PubMed ID

16263802 (在PubMed

]

文摘

内耳的腔内淋巴的Na +异常低浓度,这对转导过程是很重要的。我们最近发现,糖皮质激素受体(GR)刺激半规管的Na +吸收管(SCCD)上皮细胞。在目前的研究中,我们试图确定的基因在控制老鼠SCCD amiloride-sensitive Na +运输途径的上皮细胞和他们的表达水平是否受糖皮质激素使用实时定量rt - pcr。记录存在α-、β-和gamma-subunits上皮钠通道(钠);beta1 alpha3α1——————,和beta3-isoforms Na + - k + atp酶;短路电流的整流钾通道(IC50 Ba2 + (Isc): 210 microM] Kir2.1, Kir2.2, Kir2.3, Kir2.4, Kir3.1, Kir3.3, Kir4.1, Kir4.2, Kir5.1, Kir7.1;磺酰脲受体1 (SUR1);GR;盐皮质激素受体(MR);11 beta-hydroxysteroid脱氢酶(11 beta-hsd)类型1和2; serum- and glucocorticoid-regulated kinase 1 (Sgk1); and neural precursor cell-expressed developmentally downregulated 4-2 (Nedd4-2). On the other hand, transcripts for the alpha4-subunit of Na+-K+-ATPase, Kir1.1, Kir3.2, Kir3.4, Kir6.1, Kir6.2, and SUR2 were found to be absent, and Isc was not inhibited by glibenclamide. Dexamethasone (100 nM for 24 h) not only upregulated the transcript expression of alpha-ENaC (approximately 4-fold), beta2-subunit (approximately 2-fold) and beta3-subunit (approximately 8-fold) of Na+-K+-ATPase, Kir2.1 (approximately 5-fold), Kir2.2 (approximately 9-fold), Kir2.4 (approximately 3-fold), Kir3.1 (approximately 3- fold), Kir3.3 (approximately 2-fold), Kir4.2 (approximately 3-fold), Kir7.1 (approximately 2-fold), Sgk1 (approximately 4-fold), and Nedd4-2 (approximately 2-fold) but also downregulated GR (approximately 3-fold) and 11beta-HSD1 (approximately 2-fold). Expression of GR and 11beta-HSD1 was higher than MR and 11beta-HSD2 in the absence of dexamethasone. Dexamethasone altered transcript expression levels (alpha-ENaC and Sgk1) by activation of GR but not MR. Proteins were present for the alpha-, beta-, and gamma-subunits of ENaC and Sgk1, and expression of alpha- and gamma-ENaC was upregulated by dexamethasone. These findings are consistent with the genomic stimulation by glucocorticoids of Na+ absorption by SCCD and provide an understanding of the therapeutic action of glucocorticoids in the treatment of Meniere's disease.

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药物靶点

药物	目标	类	生物	药理作用	行动
Glymidine	ATP-sensitive内向整流钾通道1	蛋白质	人类	是的	其他/未知	细节