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The TMEM16A chloride channel as an alternative therapeutic target in cystic fibrosis
Institution:1. University of Lisboa, Faculty of Sciences, BioISI - Biosystems & Integrative Sciences Institute, Campo Grande, C8, 1749-016 Lisboa, Portugal;2. Institut für Physiologie, Universität Regensburg, Universitätsstraße 31, D-93053 Regensburg, Germany;3. Department of Medical Biotechnology and Translational Medicine, University of Milano, Milano, Italy;1. Physics Institute, Universidad Autónoma de San Luis Potosí, Ave. Dr. Manuel Nava #6, San Luis Potosí SLP 78290, Mexico;2. Department of Physiology and Biophysics, Universidad Autónoma de San Luis Potosí School of Medicine, Ave. V. Carranza 2405, San Luis Potosí SLP 78210, Mexico.
Abstract:Cystic fibrosis (CF), a multiorgan genetic disease, is caused by loss of function of CFTR, a cAMP-regulated anion channel. In CF airway epithelia, defective Cl? and bicarbonate secretion impairs mucociliary clearance and other innate defense mechanisms, favoring the colonization of the lungs by highly virulent bacteria. The airway epithelium expresses TMEM16A, a second type of Cl? channel that is activated by cytosolic Ca2+. TMEM16A is particularly expressed in goblet cells. This specific localization could be important in the release and hydration of mucins. Activation of TMEM16A with pharmacological agents could circumvent the primary defect in CF. This strategy needs to be carefully designed and tested to avoid possible undesired effects due to the expression of TMEM16A in other cell types such as bronchial smooth muscle cells.This article is part of a Directed Issue entitled: Cystic Fibrosis: From o-mics to cell biology, physiology, and therapeutic advances.
Keywords:Cystic fibrosis  Airway epithelium  Chloride secretion  Mucociliary clearance  Goblet cell
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