Renoguanylin stimulates apical CFTR translocation and decreases HCO3-secretion through PKA activity in the Gulf toadfish (Opsanus beta)
Autor: | Kevin L. Schauer, Ilan M. Ruhr, Yoshio Takei, Martin Grosell |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Gulf toadfish Physiology Guanylin Aquatic Science 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine SLC26A6 Protein kinase A Cyclic guanosine monophosphate Guanylin peptides Molecular Biology Ecology Evolution Behavior and Systematics biology PKG Apical membrane biology.organism_classification Seawater teleost Cystic fibrosis transmembrane conductance regulator Cell biology Intestine 030104 developmental biology chemistry Insect Science biology.protein Animal Science and Zoology Cl-secretion 030217 neurology & neurosurgery Uroguanylin |
Zdroj: | Ruhr, I M, Schauer, K L, Takei, Y & Grosell, M 2018, ' Renoguanylin stimulates apical CFTR translocation and decreases HCO 3-secretion through PKA activity in the Gulf toadfish (Opsanus beta) ', Journal of Experimental Biology, vol. 221, no. 6, jeb.173948 . https://doi.org/10.1242/jeb.173948 |
Popis: | The guanylin peptides - guanylin, uroguanylin and renoguanylin (RGN) - are endogenously produced hormones in teleost fish enterocytes that are activators of guanylyl cyclase-C (GC-C) and are potent modulators of intestinal physiology, particularly in seawater teleosts. Most notably, they reverse normal net ion-absorbing mechanisms that are vital to water absorption, an important process for seawater teleost survival. The role of guanylin-peptide stimulation of the intestine remains unclear, but it is hypothesized to facilitate the removal of solids from the intestine by providing fluid to enable their removal by peristalsis. The present study used one member of this group of peptides - RGN - to provide evidence for the prominent role that protein kinase A (PKA) plays in mediating the effects of guanylinpeptide stimulation in the posterior intestine of the Gulf toadfish (Opsanus beta). Protein kinase G was found to not mediate the intracellular effects of RGN, despite previous evidence showing that GC-C activation leads to higher cyclic guanosine monophosphate formation. RGN reversed the absorptive short-circuit current and increased conductance in the Gulf toadfish intestine. These effects are correlated to increased trafficking of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel to the apical membrane, which is negated by PKA inhibition. Moreover, RGN decreased HCO3-secretion, likely by limiting apical HCO3 -/Cl- exchange (possibly by reducing SLC26a6 activity), a reduction that was enhanced by PKA inhibition. RGN seems to alter PKA activity in the posterior intestine to recruit CFTR to the apical membrane and reduce HCO3-secretion. |
Databáze: | OpenAIRE |
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