PUBLICATION
A role for sodium-chloride cotransporters in the rapid regulation of ion uptake following acute environmental acidosis: New insights from the zebrafish model
- Authors
- Kwong, R.W., Perry, S.F.
- ID
- ZDB-PUB-161028-10
- Date
- 2016
- Source
- American journal of physiology. Cell physiology 311(6): C931-C941 (Journal)
- Registered Authors
- Perry, Steve F.
- Keywords
- acidosis, chloride, ionic regulation, sodium, zebrafish
- MeSH Terms
-
- Acidosis/metabolism*
- Animals
- Chlorides/metabolism
- Ions/metabolism*
- Protein Isoforms/metabolism
- Proton-Translocating ATPases/metabolism
- Sodium/metabolism
- Sodium Chloride Symporters/metabolism*
- Sodium-Hydrogen Exchangers/metabolism*
- Zebrafish/metabolism*
- Zebrafish Proteins/metabolism*
- PubMed
- 27784676 Full text @ Am. J. Physiol. Cell Physiol.
Citation
Kwong, R.W., Perry, S.F. (2016) A role for sodium-chloride cotransporters in the rapid regulation of ion uptake following acute environmental acidosis: New insights from the zebrafish model. American journal of physiology. Cell physiology. 311(6):C931-C941.
Abstract
The effects of acute exposure to acidic water on Na+ and Cl- homeostasis, and the mechanisms underlying their compensatory regulation, were investigated in the larval zebrafish Danio rerio Exposure to acidic water (pH 4.0; control pH 7.6) for 2 h significantly reduced Na+ uptake and whole body Na+ content. Nevertheless, the capacity for Na+ uptake was substantially increased in fish preexposed to acidic water but measured in control water. Based on the accumulation of the Na+-selective dye, Sodium Green, two ionocyte subtypes exhibited intracellular Na+ enrichment after preexposure to acidic water: H+-ATPase rich (HR) cells, which coexpress the Na+/H+ exchanger isoform 3b (NHE3b), and a non-HR cell population. In fish experiencing Na+-Cl- cotransporter (NCC) knockdown, we observed no Sodium Green accumulation in the latter cell type, suggesting the non-HR cells were NCC cells. Elimination of NHE3b-expressing HR cells did not prevent the increased Na+ uptake following acid exposure. On the other hand, the increased Na+ uptake was abolished when the acidic water was enriched with Na+ and Cl-, but not with Na+ only, indicating that the elevated Na+ uptake after acid exposure was associated with the compensatory regulation of Cl- Further examinations demonstrated that acute acid exposure also reduced whole body Cl- levels and increased the capacity for Cl- uptake. Moreover, knockdown of NCC prevented the increased uptake of both Na+ and Cl- after exposure to acidic water. Together, the results of the present study revealed a novel role of NCC in the compensatory regulation of Na+ and Cl- uptake following acute acidosis.
Genes / Markers
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping