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首页> 美国卫生研究院文献>American Journal of Physiology - Cell Physiology >Deletion of the anion exchanger Slc26a4 (pendrin) decreases apical Cl−/HCO3− exchanger activity and impairs bicarbonate secretion in kidney collecting duct
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Deletion of the anion exchanger Slc26a4 (pendrin) decreases apical Cl−/HCO3− exchanger activity and impairs bicarbonate secretion in kidney collecting duct

机译：删除阴离子交换剂Slc26a4（苯endrin）会降低顶端Cl- / HCO3-交换子的活性并损害肾脏收集管中的碳酸氢盐分泌

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The anion exchanger Pendrin, which is encoded by SLC26A4 (human)/Slc26a4 (mouse) gene, is localized on the apical membrane of non-acid-secreting intercalated (IC) cells in the kidney cortical collecting duct (CCD). To examine its role in the mediation of bicarbonate secretion in vivo and the apical Cl−/HCO3− exchanger in the kidney CCD, mice with genetic deletion of pendrin were generated. The mutant mice show the complete absence of pendrin expression in their kidneys as assessed by Northern blot hybridization, Western blot, and immunofluorescence labeling. Pendrin knockout (KO) mice display significantly acidic urine at baseline [pH 5.20 in KO vs. 6.01 in wild type (WT); P < 0.0001] along with elevated serum HCO3− concentration (27.4 vs. 24 meq/l in KO vs. WT, respectively; P < 0.02), consistent with decreased bicarbonate secretion in vivo. The urine chloride excretion was comparable in WT and KO mice. For functional studies, CCDs were microperfused and IC cells were identified by their ability to trap the pH fluorescent dye BCECF. The apical Cl−/HCO3− exchanger activity in B-IC and non-A, non-B-IC cells, as assessed by intracellular pH monitoring, was significantly reduced in pendrin-null mice. The basolateral Cl−/HCO3− exchanger activity in A-IC cells and in non-A, non-B-IC cells, was not different in pendrin KO mice relative to WT animals. Urine NH4+ (ammonium) excretion increased significantly, consistent with increased trapping of NH3 in the collecting duct in pendrin KO mice. We conclude that Slc26a4 (pendrin) deletion impairs the secretion of bicarbonate in vivo and reduces apical Cl−/HCO3− exchanger activity in B-IC and non-A, non-B-IC cells in CCD. Additional apical Cl−/HCO3− exchanger(s) is (are) present in the CCD.
机译：由SLC26A4（人类）/ Slc26a4（小鼠）基因编码的阴离子交换体Pendrin定位于肾皮质收集管（CCD）中非酸性分泌层间（IC）细胞的顶膜上。为了检查其在体内碳酸氢盐分泌的介导和肾脏CCD中顶端Cl - / HCO3 -交换子中的作用，生成了具有Pendrin基因缺失的小鼠。通过Northern杂交，Western印迹和免疫荧光标记评估，突变小鼠的肾脏中完全没有Pendrin表达。 Pendrin基因敲除（KO）小鼠在基线时显示出明显的酸性尿液[KO中的pH 5.20与野生型（WT）中的6.01； P <0.0001]以及血清HCO3 -浓度升高（KO vs. WT分别为27.4 vs. 24 meq / l； P <0.02），与体内碳酸氢盐分泌减少有关。 WT和KO小鼠的尿氯化物排泄量相当。为了进行功能研究，对CCD进行了微灌流，并通过捕获pH荧光染料BCECF的能力鉴定了IC细胞。通过细胞内pH监测，B-IC和非A，非B-IC细胞的顶端Cl - / HCO3 -交换子活性显着降低。零蛋白的小鼠。与Pendrin KO小鼠相比，A-IC细胞和非A，非B-IC细胞的基底外侧Cl - / HCO3 -交换子活性没有差异野生动物。尿液中NH4 + （铵）的排泄量显着增加，这与pendrin KO小鼠收集管中的NH3捕集增加有关。我们得出的结论是，Slc26a4（pendrin）缺失会损害体内碳酸氢盐的分泌，并降低B-IC和非A，非A-中的根尖Cl - / HCO3 -交换子的活性。 CCD中的B-IC细胞。 CCD中还存在其他顶端Cl - / HCO3 -交换剂。

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