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

Chang WJ, Wang YF, Hu HJ, Wang JH, Lee TH, Hwang PP - Front. Zool. (2013)

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan. pphwang@gate.sinica.edu.tw.

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.

No MeSH data available.


Related in: MedlinePlus

Effect of ncc knockdown on Na+ accumulation in zebrafish larvae under acid stress. (A, B): Whole body Na+ content in wild type (WT) larvae and ncc morphants (MO) treated with control pH7 or acidic pH4 FW for 3 d (A) or 4 d (B). Mean ± SD (n = 6). *p < 0.05 (Student’s t-test). abcsignificant difference (One-way ANOVA, Tukey’s multiple-comparison).
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Figure 7: Effect of ncc knockdown on Na+ accumulation in zebrafish larvae under acid stress. (A, B): Whole body Na+ content in wild type (WT) larvae and ncc morphants (MO) treated with control pH7 or acidic pH4 FW for 3 d (A) or 4 d (B). Mean ± SD (n = 6). *p < 0.05 (Student’s t-test). abcsignificant difference (One-way ANOVA, Tukey’s multiple-comparison).

Mentions: The whole body Na+ contents of wild type larvae and ncc morphants were compared after treatment with pH 7 (control) or pH 4 FW. The Na+ contents of wild type and ncc morphants maintained in pH 7 FW were not significantly different (Figure 7A, B). However, the Na+ content in 3 dpf ncc morphants was lower (albeit not significantly) than that in wild type larvae upon acid stress; this decrease was greater and significant at 4 dpf (Figure 7A, B), suggesting that NCC is necessary for the compensatory regulation of Na+ absorption during acid acclimation.


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

Chang WJ, Wang YF, Hu HJ, Wang JH, Lee TH, Hwang PP - Front. Zool. (2013)

Effect of ncc knockdown on Na+ accumulation in zebrafish larvae under acid stress. (A, B): Whole body Na+ content in wild type (WT) larvae and ncc morphants (MO) treated with control pH7 or acidic pH4 FW for 3 d (A) or 4 d (B). Mean ± SD (n = 6). *p < 0.05 (Student’s t-test). abcsignificant difference (One-way ANOVA, Tukey’s multiple-comparison).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3750650&req=5

Figure 7: Effect of ncc knockdown on Na+ accumulation in zebrafish larvae under acid stress. (A, B): Whole body Na+ content in wild type (WT) larvae and ncc morphants (MO) treated with control pH7 or acidic pH4 FW for 3 d (A) or 4 d (B). Mean ± SD (n = 6). *p < 0.05 (Student’s t-test). abcsignificant difference (One-way ANOVA, Tukey’s multiple-comparison).
Mentions: The whole body Na+ contents of wild type larvae and ncc morphants were compared after treatment with pH 7 (control) or pH 4 FW. The Na+ contents of wild type and ncc morphants maintained in pH 7 FW were not significantly different (Figure 7A, B). However, the Na+ content in 3 dpf ncc morphants was lower (albeit not significantly) than that in wild type larvae upon acid stress; this decrease was greater and significant at 4 dpf (Figure 7A, B), suggesting that NCC is necessary for the compensatory regulation of Na+ absorption during acid acclimation.

Bottom Line: 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.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan. pphwang@gate.sinica.edu.tw.

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.

No MeSH data available.


Related in: MedlinePlus