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斑马鱼（Danio rerio）中 Na+/H+ 交换器和 Na+-Cl- 共转运蛋白对 Na+ 吸收的代偿调节。

Compensatory regulation of Na+ absorption by Na+/H+ exchanger and Na+-Cl- cotransporter in zebrafish (Danio rerio).

机构信息

Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan.

出版信息

Front Zool. 2013 Aug 7;10(1):46. doi: 10.1186/1742-9994-10-46.

DOI:10.1186/1742-9994-10-46
PMID:23924428
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3750650/
Abstract

INTRODUCTION

In mammals, internal Na+ homeostasis is maintained through Na+ reabsorption via a variety of Na+ transport proteins with mutually compensating functions, which are expressed in different segments of the nephrons. In zebrafish, Na+ homeostasis is achieved mainly through the skin/gill ionocytes, namely Na+/H+ exchanger (NHE3b)-expressing H+-ATPase rich (HR) cells and Na+-Cl- cotransporter (NCC)-expressing NCC cells, which are functionally homologous to mammalian proximal and distal convoluted tubular cells, respectively. The present study aimed to investigate whether or not the functions of HR and NCC ionocytes are differentially regulated to compensate for disruptions of internal Na+ homeostasis and if the cell differentiation of the ionocytes is involved in this regulation pathway.

RESULTS

Translational knockdown of ncc caused an increase in HR cell number and a resulting augmentation of Na+ uptake in zebrafish larvae, while NHE3b loss-of-function caused an increase in NCC cell number with a concomitant recovery of Na+ absorption. Environmental acid stress suppressed nhe3b expression in HR cells and decreased Na+ content, which was followed by up-regulation of NCC cells accompanied by recovery of Na+ content. Moreover, knockdown of ncc resulted in a significant decrease of Na+ content in acid-acclimated zebrafish.

CONCLUSIONS

These results provide evidence that HR and NCC cells exhibit functional redundancy in Na+ absorption, similar to the regulatory mechanisms in mammalian kidney, and suggest this functional redundancy is a critical strategy used by zebrafish to survive in a harsh environment that disturbs body fluid Na+ homeostasis.

摘要

简介

在哺乳动物中，通过多种具有相互补偿功能的 Na+转运蛋白，Na+的重吸收维持了细胞内的 Na+稳态，这些蛋白在肾单位的不同节段表达。在斑马鱼中，Na+稳态主要通过皮肤/鳃离子细胞来实现，即表达 Na+/H+交换蛋白（NHE3b）的 H+-ATPase 丰富（HR）细胞和表达 Na+-Cl-共转运蛋白（NCC）的 NCC 细胞，它们分别与哺乳动物的近端和远端卷曲状肾小管细胞在功能上同源。本研究旨在探讨 HR 和 NCC 离子细胞的功能是否通过差异调节来补偿细胞内 Na+稳态的破坏，以及离子细胞的细胞分化是否参与这一调节途径。

结果

ncc 的翻译抑制导致斑马鱼幼虫 HR 细胞数量增加，Na+摄取增加，而 NHE3b 功能丧失导致 NCC 细胞数量增加，同时 Na+吸收恢复。环境酸性胁迫抑制 HR 细胞中 nhe3b 的表达，降低 Na+含量，随后 NCC 细胞上调，Na+含量恢复。此外，ncc 的敲低导致酸适应的斑马鱼中 Na+含量显著降低。

结论

这些结果提供了证据表明，HR 和 NCC 细胞在 Na+吸收方面表现出功能冗余，类似于哺乳动物肾脏的调节机制，并表明这种功能冗余是斑马鱼在扰乱体液 Na+稳态的恶劣环境中生存的关键策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66eb/3750650/0a49e450484b/1742-9994-10-46-7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66eb/3750650/5cff54712941/1742-9994-10-46-1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/66eb/3750650/5cff54712941/1742-9994-10-46-1.jpg
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