Wild type but not ΔF508 CFTR inhibits Na+ conductance when coexpressed in Xenopus oocytes

124Citations
Citations of this article
21Readers
Mendeley users who have this article in their library.

Abstract

Airway epithelial cells bearing mutations of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) possess an increased Na+ conductance along with their well described defect of cAMP dependent Cl- conductance. Currently it is not clear, how this occurs, and whether it is due to a CFTR control of epithelial Na+ conductances which might be defective in CF patients. In the present study, we have tried to identify possible interactions between both CFTR and the epithelial Na+ conductance by overexpressing respective cRNAs in Xenopus oocytes. The expression of all three (α, β, γ) subunits of the rat epithelial Na+ channel (rENaC) and wild type (wt) CFTR resulted in the expected amiloride sensitive Na+ and IBMX (1 mmol/l) activated Cl- currents, respectively. The amiloride sensitive Na+ conductance was, however, inhibited when the wt-CFTR Cl- conductance was activated by phosphodiesterase inhibition (IBMX). In contrast, IBMX had no such effect in ΔF508 and Na+ channels coexpressing oocytes. These results suggest that wt-CFTR, but not ΔF508-CFTR, is a cAMP dependent downregulator of epithelial Na+ channels. This may explain the higher Na+ conductance observed in airway epithelial cells of CF patients.

Cite

CITATION STYLE

APA

Mall, M., Hipper, A., Greger, R., & Kunzelmann, K. (1996). Wild type but not ΔF508 CFTR inhibits Na+ conductance when coexpressed in Xenopus oocytes. FEBS Letters, 381(1–2), 47–52. https://doi.org/10.1016/0014-5793(96)00079-8

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free