ZFIN ID: ZDB-PUB-120807-9
Evidence for a role of tight junctions in regulating sodium permeability in zebrafish (Danio rerio) acclimated to ion-poor water
Kwong, R.W., Kumai, Y., and Perry, S.F.
Date: 2013
Source: Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology   183(2): 203-213 (Journal)
Registered Authors: Perry, Steve F.
Keywords: gill, ion homeostasis, kidney, epithelial permeability, tight junction, zebrafish
MeSH Terms:
  • Acclimatization/physiology*
  • Animals
  • Blotting, Western
  • Claudins/metabolism*
  • DNA Primers/genetics
  • Fresh Water/chemistry*
  • Immunohistochemistry
  • Kidney Tubules, Collecting/metabolism
  • Permeability
  • Polyethylene Glycols
  • Real-Time Polymerase Chain Reaction
  • Sodium/analysis
  • Sodium/metabolism*
  • Sodium-Potassium-Exchanging ATPase/metabolism
  • Tight Junctions/metabolism
  • Tight Junctions/physiology*
  • Zebrafish/physiology*
PubMed: 22843140 Full text @ J. Comp. Physiol. B
ABSTRACT

Freshwater teleosts are challenged by diffusive ion loss across permeable epithelia including gills and skin. Although the mechanisms regulating ion loss are poorly understood, a significant component is thought to involve paracellular efflux through pathways formed via tight junction proteins. The mammalian orthologue (claudin-4) of zebrafish (Danio rerio) tight junction protein, claudin-b, has been proposed to form a cation-selective barrier regulating the paracellular loss of Na+. The present study investigated the cellular localization and regulation of claudin-b, as well as its potential contribution to Na+ homeostasis in adult zebrafish acclimated to ion-poor water. Using a green fluorescent protein-expressing line of transgenic zebrafish, we found that claudin-b was expressed along the lamellar epithelium as well as on the filament in the inter-lamellar regions. Co-localization of claudin-b and Na+/K+-ATPase was observed, suggesting its interaction with mitochondrion-rich cells. Claudin-b also appeared to be associated with other cell types, including the pavement cells. In the kidney, claudin-b was expressed predominantly in the collecting tubules. In addition, exposure to ion-poor water caused a significant increase in claudin-b abundance as well as a decrease in Na+ efflux, suggesting a possible role for claudin-b in regulating paracellular Na+ loss. Interestingly, the whole-body uptake of a paracellular permeability marker, polyethylene glycol-400, increased significantly after prolonged exposure to ion-poor water, indicating that an increase in epithelial permeability is not necessarily coupled with an increase in passive Na+ loss. Overall, our study suggests that in ion-poor conditions, claudin-b may contribute to a selective reduction in passive Na+ loss in zebrafish.

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