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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

Knockdown of ncc increases HR cell number and Na+ accumulation. (A, B): H+-ATPase (H-pump) immunostaining signals (arrow) in 4-dpf wild type larvae (WT) and ncc morphants. Scale bar = 100 μm. (C, D): Comparisons of HR cell density (C) and whole body Na+ content (D) between wild type larvae (white bars) and ncc morphants (gray bars) at different developmental stages (n = 8 in C and 6 in D). Mean ± SD. *p < 0.05; **p < 0.01; ***p < 0.001 (Student’s t-test).
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Figure 1: Knockdown of ncc increases HR cell number and Na+ accumulation. (A, B): H+-ATPase (H-pump) immunostaining signals (arrow) in 4-dpf wild type larvae (WT) and ncc morphants. Scale bar = 100 μm. (C, D): Comparisons of HR cell density (C) and whole body Na+ content (D) between wild type larvae (white bars) and ncc morphants (gray bars) at different developmental stages (n = 8 in C and 6 in D). Mean ± SD. *p < 0.05; **p < 0.01; ***p < 0.001 (Student’s t-test).

Mentions: Compensatory expression of Na+ transporters was previously observed in NCC mice [9]. In order to identify whether similar compensation occurs in zebrafish, the development of HR cells was observed in ncc morphants. As shown in Figure 1A-C, knockdown of NCC translation enhanced differentiation of HR cells in 4- and 5 dpf larvae. The Na+ content remained at wild type levels in 2- and 3 dpf morphants, but was significantly increased in 5- and 6 dpf larvae (Figure 1D). Initially, NCC loss-of-function does not significantly affect Na+ accumulation, but by later stages, Na+ accumulation is enhanced. This may be due to an accompanying increase of HR cells, which express the major Na+-uptake transporter, NHE3b. This suggests that an increase of HR cells (and thus NHE3b expression) may compensate for the loss of NCC in terms of Na+ uptake.


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)

Knockdown of ncc increases HR cell number and Na+ accumulation. (A, B): H+-ATPase (H-pump) immunostaining signals (arrow) in 4-dpf wild type larvae (WT) and ncc morphants. Scale bar = 100 μm. (C, D): Comparisons of HR cell density (C) and whole body Na+ content (D) between wild type larvae (white bars) and ncc morphants (gray bars) at different developmental stages (n = 8 in C and 6 in D). Mean ± SD. *p < 0.05; **p < 0.01; ***p < 0.001 (Student’s t-test).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 1: Knockdown of ncc increases HR cell number and Na+ accumulation. (A, B): H+-ATPase (H-pump) immunostaining signals (arrow) in 4-dpf wild type larvae (WT) and ncc morphants. Scale bar = 100 μm. (C, D): Comparisons of HR cell density (C) and whole body Na+ content (D) between wild type larvae (white bars) and ncc morphants (gray bars) at different developmental stages (n = 8 in C and 6 in D). Mean ± SD. *p < 0.05; **p < 0.01; ***p < 0.001 (Student’s t-test).
Mentions: Compensatory expression of Na+ transporters was previously observed in NCC mice [9]. In order to identify whether similar compensation occurs in zebrafish, the development of HR cells was observed in ncc morphants. As shown in Figure 1A-C, knockdown of NCC translation enhanced differentiation of HR cells in 4- and 5 dpf larvae. The Na+ content remained at wild type levels in 2- and 3 dpf morphants, but was significantly increased in 5- and 6 dpf larvae (Figure 1D). Initially, NCC loss-of-function does not significantly affect Na+ accumulation, but by later stages, Na+ accumulation is enhanced. This may be due to an accompanying increase of HR cells, which express the major Na+-uptake transporter, NHE3b. This suggests that an increase of HR cells (and thus NHE3b expression) may compensate for the loss of NCC in terms of Na+ uptake.

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