Regulation of the Epithelial Sodium Channel (ENaC) by the Short Palate, Lung, and Nasal Epithelial Clone (SPLUNC1)
Public Deposited- Last Modified
- March 20, 2019
- Creator
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Rollins, Brett
- Affiliation: School of Medicine, Department of Cell Biology and Physiology
- Abstract
- The airways rely on mucociliary clearance (MCC) to remove inhaled particulates. Initiating events in chronic airway diseases, such as cystic fibrosis (CF), have been traced back to the failure of a critical MCC component, ion transport. Specifically, the epithelial sodium channel (ENaC) is known to be hyperabsorptive in CF airway epithelia and contributes to dehydrated airway surface liquid (ASL), collapsed cilia, and high percent solid mucus. Recently, proteolytic cleavage and activation of ENaC has been described and SPLUNC1 was identified as an endogenous inhibitor of ENaC activation. Here, we demonstrate SPLUNC1's ability to reduce macroscopic current and specifically the number of channels of membrane-inserted ENaCs. This work also identifies the active site of SPLUNC1 and provides evidence for a functional SPLUNC1 mimetic peptide. Further, as nonfunctional CFTR influences abnormal bicarbonate secretion and thus CF ASL pH, we correlated the loss of SPLUNC1's function in CF airways to this acidic environment.
- Date of publication
- December 2010
- Keyword
- DOI
- Resource type
- Rights statement
- In Copyright
- Advisor
- Tarran, Robert
- Lund, Pauline Kay
- Anderson, James M.
- Degree
- Master of Science
- Degree granting institution
- University of North Carolina at Chapel Hill Graduate School
- Graduation year
- 2010
- Language
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This work has no parents.
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