Decreased expression of Slc26a4 (Pendrin) and Slc26a7 in the kidneys of carbonic anhydrase II-deficient mice.
Decreased expression of Slc26a4 (Pendrin) and Slc26a7 in the kidneys of carbonic anhydrase II-deficient mice.
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碳酸酐酶 II 缺陷小鼠肾脏中 Slc26a4 (Pendrin) 和 Slc26a7 的表达降低。
DOI：
10.1159/000113751
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
Petrovic,Snezana
中科院分区：
文献类型：
--
作者：
Sun,Xuming;Soleimani,Manoocher;Petrovic,Snezana
背景/目标：肾集合管的嵌入细胞（IC）富含碳酸酐酶II（CAII），其促进质子和碳酸氢盐转运。Bicycline分泌通过Pendrin（Slc 26 a4）介导，Pendrin（Slc 26 a4）在皮质集合管（CCD）中的B-IC和非A-非B IC的顶膜上表达。在CCD中通过阴离子交换剂1（AE 1-Slc 4a 1）以及在OMCD中通过AE 1和可能的Slc 26 a7介导重离子吸收。两种交换剂均在A-IC的基底外侧膜上表达。本研究的目的是检查pendrin，Slc 26 a7和AE 1在CAII缺陷（CAR 2-null）小鼠肾脏中的表达。方法：采用实时荧光定量RT-PCR、北方杂交、免疫标记和免疫印迹技术进行表达研究。结果如下：Pendrin mRNA表达降低了63%沿着减少的Pendrin免疫标记在CAR 2缺失小鼠的皮质中主要存在于非A-非B IC中。Slc 26 a7 mRNA表达降低了73%，并且存在于A-IC中的Slc 26 a7免疫标记在CAR 2缺失小鼠的外髓质中严重减少。随着AE 1免疫标记的减少，AE 1 mRNA表达降低至相似程度（62%）沿着降低。水通道蛋白2（AQP 2）水通道的表达仅存在于集合管的主细胞中，在野生型和CAR 2缺失小鼠中相当。结论：CAII缺乏导致来自Slc 26基因家族的碳酸氢盐转运蛋白-Slc 26 a4（pendrin）和Slc 26 a7的基因和蛋白表达显著降低。这些结果强调了CAII对于维持闰细胞表型的关键作用。
Background/Aims: Intercalated cells (ICs) of the kidney collecting duct are rich in carbonic anhydrase II (CAII), which facilitates proton and bicarbonate transport. Bicarbonate secretion is mediated via Pendrin (Slc26a4), which is expressed on the apical membrane of B-ICs and nonA-nonB ICs in the cortical collecting ducts (CCD). Bicarbonate absorption is mediated via anion exchanger 1 (AE1-Slc4a1) in the CCD and via AE1 and possibly Slc26a7 in the OMCD. Both exchangers are expressed on the basolateral membrane of A-ICs. The aim of this study was to examine the expression of pendrin, Slc26a7, and AE1 in the kidneys of CAII-deficient (CAR2-null) mice. Methods: For the expression studies, we used real-time RT-PCR, Northern hybridization, immunolabeling, and immunoblotting. Results: Pendrin mRNA expression was reduced 63% along with decreased pendrin immunolabeling in the cortex of CAR2-null mice present predominantly in nonA-nonB ICs. Slc26a7 mRNA expression was decreases by 73% and Slc26a7 immunolabeling, present in A-ICs, severely reduced in the outer medulla of CAR2-null mice. AE1 mRNA expression was decreased to a similar degree (62%) along with reduced AE1 immunolabeling. The expression of aquaporin 2 (AQP2) water channel, exclusively present in principal cells of the collecting duct, was comparable in the wild type and CAR2-null mice. Conclusion: CAII deficiency results in a significant decrease in the gene and protein expression of bicarbonate transport proteins from Slc26 gene family – Slc26a4 (pendrin) and Slc26a7. These results emphasize the critical role of CAII for the maintenance of the intercalated cell phenotype.