Endothelin-1 regulates H+-ATPase-dependent transepithelial H+ secretion in zebrafish
- Authors
- Guh, Y.J., Tseng, Y.C., Yang, C.Y., and Hwang, P.P.
- ID
- ZDB-PUB-140318-8
- Date
- 2014
- Source
- Endocrinology 155(5): 1728-37 (Journal)
- Registered Authors
- Guh, Ying-Jey, Hwang, Pung Pung, Tseng, Yung-Che
- Keywords
- none
- MeSH Terms
-
- Acid-Base Equilibrium/drug effects
- Animals
- Biological Transport, Active/drug effects
- Endothelin A Receptor Antagonists
- Endothelin-1/biosynthesis
- Endothelin-1/genetics
- Endothelin-1/metabolism*
- Enzyme Inhibitors/pharmacology
- Female
- Gene Expression Regulation, Developmental/drug effects
- Hydrogen-Ion Concentration
- Macrolides/pharmacology
- Male
- Membrane Transport Modulators/pharmacology
- Morpholinos/pharmacology
- Protein Subunits/antagonists & inhibitors
- Protein Subunits/genetics
- Protein Subunits/metabolism
- Receptor, Endothelin A/genetics
- Receptor, Endothelin A/metabolism*
- Signal Transduction*/drug effects
- Skin/drug effects
- Skin/embryology
- Skin/metabolism
- Sodium-Hydrogen Exchangers/antagonists & inhibitors
- Sodium-Hydrogen Exchangers/metabolism
- Vacuolar Proton-Translocating ATPases/antagonists & inhibitors
- Vacuolar Proton-Translocating ATPases/genetics
- Vacuolar Proton-Translocating ATPases/metabolism*
- Zebrafish/embryology
- Zebrafish/metabolism*
- Zebrafish Proteins/antagonists & inhibitors
- Zebrafish Proteins/biosynthesis
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 24424055 Full text @ Endocrinology
Endothelin-1 (EDN1) is an important regulator of H+ secretion in the mammalian kidney. EDN1 enhances renal tubule H+-ATPase activity, but the underlying mechanism remains unclear. To further elucidate the role of EDN1 in vertebrates' acid-base regulation, the present study used zebrafish as the model to examine the effects of EDN1 and its receptors on transepithelial H+ secretion. Expression of EDN1 and one of its receptors, EDNRAa, was stimulated in zebrafish acclimated to acidic water. A non-invasive scanning ion-selective electrode technique was used to show that edn1 overexpression enhances H+ secretion in embryonic skin at 3 days post fertilization. EDNRAa loss-of-function significantly decreased EDN1- and acid-induced H+ secretion. Abrogation of EDN1-enhanced H+ secretion by a vacuolar H+-ATPase inhibitor (bafilomycin A1) suggests that EDN1 exerts its action by regulating the H+-ATPase-mediated H+ secretion. EDN1 does not appear to affect H+ secretion through either altering the abundance of H+-ATPase or affecting the cell differentiation of H+-ATPase-rich (HR) ionocytes, because the reduction in secretion upon ednraa knockdown was not accompanied by decreased expression of H+-ATPase or reduced HR cell density. These findings provide evidence that EDN1 signaling is involved in acid-base regulation in zebrafish, and enhance our understanding of EDN1 regulation of transepithelial H+ secretion in vertebrates.