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The Epithelial Sodium Channel (ENaC) Establishes a Trafficking Vesicle Pool Responsible for Its Regulation

Edinger, RS and Bertrand, CA and Rondandino, C and Apodaca, GA and Johnson, JP and Butterworth, MB (2012) The Epithelial Sodium Channel (ENaC) Establishes a Trafficking Vesicle Pool Responsible for Its Regulation. PLoS ONE, 7 (9).

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The epithelial sodium channel (ENaC) is the rate-limiting step for sodium reabsorption across tight epithelia. Cyclic-AMP (cAMP) stimulation promotes ENaC trafficking to the apical surface to increase channel number and transcellular Na+ transport. Removal of corticosteroid supplementation in a cultured cortical collecting duct cell line reduced ENaC expression. Concurrently, the number of vesicles trafficked in response to cAMP stimulation, as measured by a change in membrane capacitance, also decreased. Stimulation with aldosterone restored both the basal and cAMP-stimulated ENaC activity and increased the number of exocytosed vesicles. Knocking down ENaC directly decreased both the cAMP-stimulated short-circuit current and capacitance response in the presence of aldosterone. However, constitutive apical recycling of the Immunoglobulin A receptor was unaffected by alterations in ENaC expression or trafficking. Fischer Rat Thyroid cells, transfected with α,β,γ-mENaC had a significantly greater membrane capacitance response to cAMP stimulation compared to non-ENaC controls. Finally, immunofluorescent labeling and quantitation revealed a smaller number of vesicles in cells where ENaC expression was reduced. These findings indicate that ENaC is not a passive passenger in regulated epithelial vesicle trafficking, but plays a role in establishing and maintaining the pool of vesicles that respond to cAMP stimulation. © 2012 Edinger et al.


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Item Type: Article
Status: Published
CreatorsEmailPitt UsernameORCID
Edinger, RSrse9@pitt.eduRSE9
Bertrand, CAcbertra@pitt.eduCBERTRA
Rondandino, C
Apodaca, GA
Johnson, JPjohnsonj@pitt.eduJOHNSONJ
Butterworth, MBmichael7@pitt.eduMICHAEL7
ContributionContributors NameEmailPitt UsernameORCID
Date: 28 September 2012
Date Type: Publication
Journal or Publication Title: PLoS ONE
Volume: 7
Number: 9
DOI or Unique Handle: 10.1371/journal.pone.0046593
Schools and Programs: School of Medicine > Cell Biology
Refereed: Yes
Other ID: NLM PMC3460899
PubMed Central ID: PMC3460899
PubMed ID: 23029554
Date Deposited: 22 Oct 2012 21:27
Last Modified: 22 Jun 2021 15:55


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