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首页> 外文期刊>American Journal of Physiology >Dietary potassium restriction stimulates endocytosis of ROMK channel in rat cortical collecting duct.
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Dietary potassium restriction stimulates endocytosis of ROMK channel in rat cortical collecting duct.

机译：饮食中钾的限制会刺激大鼠皮质收集管中ROMK通道的内吞作用。

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摘要

ROMK potassium channels are present in the cortical collecting ducts (CCDs) of the kidney and serve as the exit pathways for K+ secretion in this nephron segment. Dietary K+ restriction reduces the abundance of ROMK in the kidney. We have previously shown that ROMK undergoes endocytosis via clathrin-coated vesicles in Xenopus laevis oocytes and in cultured cells. Here, we examined the effect of dietary K+ restriction on endocytosis of ROMK in CCDs using double-labeling immunofluorescent staining and confocal microscopic imaging in whole kidney sections as well as in individually isolated tubules. We found that ROMK abundance in kidney cortex and CCDs was reduced in rats fed a K+-restricted diet compared with rats fed the control K+ diet. In the control animals, ROMK staining was preferentially localized to the apical membrane of CCDs. Compared with control tubules, ROMK staining in CCDs was markedly shifted toward intracellular locations in animals fed a K+-deficient diet for 48 h. Some of the intracellular distribution of ROMK colocalized with an early endosomal marker, early endosomal antigen-1 or with a late endosomal/lysosomal marker, lysosomal membrane glycoprotein-120. These results suggest that K+ restriction reduces the abundance of ROMK in CCDs by increasing endocytosis and degradation of the channel protein. This decrease in the abundance of ROMK is likely important for maintaining K+ homeostasis during K+ deficiency.
机译：ROMK钾通道存在于肾脏的皮质收集管（CCD）中，并充当该肾单位段中K +分泌的出口途径。饮食中的K +限制会降低肾脏中ROMK的含量。我们以前已经表明，ROMK在非洲爪蟾卵母细胞和培养细胞中通过网格蛋白包被的囊泡经历内吞作用。在这里，我们使用双标记免疫荧光染色和共聚焦显微成像在整个肾脏切片以及单个分离的肾小管中检查了饮食中K +限制对ROMK内吞作用的影响。我们发现与限制K +饮食相比，限制K +饮食的大鼠肾脏皮质和CCD的ROMK丰度降低。在对照动物中，ROMK染色优先位于CCD的顶膜。与对照肾小管相比，CCD的ROMK染色明显向缺乏K +饮食的动物48 h转移至细胞内位置。 ROMK的一些胞内分布与早期的内体标记物，早期的内体抗原-1或晚期的内体/溶酶体标记物，溶酶体膜糖蛋白-120共定位。这些结果表明，K +限制通过增加内吞作用和通道蛋白的降解而降低了CCD中ROMK的含量。 ROMK丰度的下降对于在K +缺乏期间维持K +稳态可能很重要。

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