Estrogen modulates ClC-2 chloride channel gene expression in rat kidney.
Estrogen modulates ClC-2 chloride channel gene expression in rat kidney.
复制标题
雌激素调节大鼠肾脏中 ClC-2 氯离子通道基因的表达。
DOI：
10.1007/s00424-003-1095-y
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发表时间：
2003
期刊：
影响因子：
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通讯作者：
Morales,MarceloM
中科院分区：
文献类型：
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作者：
Nascimento,DanielleS;Reis,CarlosU;Goldenberg,ReginaC;Ortiga-Carvalho,TâniaM;Pazos-Moura,CarmenC;Guggino,SandraE;Guggino,WilliamB;Morales,MarceloM
ClC-2是对细胞体积、pH和电压变化敏感的氯离子通道的CLC家族成员。ClC-2广泛分布于沿着肾单位，尽管其在肾脏中的作用仍不清楚。醛固酮研究表明，ClC-2在肾脏中的表达可能受到肾脏调节。为了探讨雌激素控制ClC-2表达的可能性，我们研究了在切除卵巢的雌性Wistar大鼠中，在有或没有接近生理或高剂量的17β-雌二醇苯甲酸酯治疗10天的情况下，ClC-2的表达是否在肾脏中发生变化。通过核糖核酸酶保护试验和/或半定量RT-PCR分析从大鼠肾脏和解剖的肾单位节段分离的总RNA。Western blot检测肾组织ClC-2蛋白表达。在卵巢切除大鼠中观察到的ClC-2 mRNA和蛋白表达的降低在低剂量雌二醇治疗后恢复到对照水平。更高剂量的雌二醇导致ClC-2 mRNA和蛋白表达的更大增加。整体表达的这种变化被证明是由近端小管中ClC-2 mRNA表达的调节引起的。这些结果表明，ClC-2可能参与雌激素诱导的大鼠肾脏Cl−转运。
ClC-2 is a CLC family member of chloride channels sensitive to changes in cell volume, pH and voltage. The ClC-2 is widely distributed along the nephron although in the kidney its role still not well understood. Aldosterone studies suggest that ClC-2 expression in the kidney may be hormonally regulated. To explore the possibility that estrogen control ClC-2 expression, we investigated whether its expression changed in the kidney of female Wistar rats subjected to ovariectomy with or without near-physiological or high doses of 17β-estradiol benzoate treatment for 10 days. Total RNA isolated from rat kidney and dissected nephron segments was analyzed by ribonuclease protection assay and/or a semi-quantitative RT-PCR. The renal ClC-2 protein expression was analyzed by Western blot. The decreased renal expression of ClC-2 mRNA and protein observed in ovariectomized rats was restored to control levels after treatment with low doses of estradiol. Higher dose estradiol lead to an even greater increase in ClC-2 mRNA and protein expression. This change in overall expression was shown to be caused by the modulation of ClC-2 mRNA expression in the proximal tubule. These results suggest that ClC-2 may be involved in estrogen-induced Cl−transport in rat kidney.