Endothelin-1 regulates H⁺-ATPase-dependent transepithelial H⁺ secretion in zebrafish
| Autor: | Ying Jey Guh, Yung Che Tseng, Pung-Pung Hwang, Chao Yew Yang |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Male
medicine.medical_specialty Vacuolar Proton-Translocating ATPases Sodium-Hydrogen Exchangers Endothelin A Receptor Antagonists ATPase Biological Transport Active Morpholinos chemistry.chemical_compound Endocrinology Internal medicine Membrane Transport Modulators medicine Animals Secretion Enzyme Inhibitors Receptor Zebrafish Skin Acid-Base Equilibrium Kidney biology Endothelin-1 Sodium-Hydrogen Exchanger 3 Bafilomycin Gene Expression Regulation Developmental Embryo Hydrogen-Ion Concentration Zebrafish Proteins biology.organism_classification Receptor Endothelin A Endothelin 1 Cell biology Protein Subunits medicine.anatomical_structure chemistry biology.protein Female Macrolides Signal Transduction |
| Zdroj: | Endocrinology. 155(5) |
| ISSN: | 1945-7170 |
| Popis: | 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 noninvasive 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 ionocytes, because the reduction in secretion upon ednraa knockdown was not accompanied by decreased expression of H+-ATPase or reduced H+-ATPase-rich 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. |
| Databáze: | OpenAIRE |
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