Chloride intracellular channel 1 (CLIC1) contributes to modulation of cyclic AMP-activated whole-cell chloride currents in human bronchial epithelial cells.

Bo Liu,Charlotte K Billington,Ian P Hall,Caroline Swan,Alexander K Kheirallah,Sangita K Bhaker,Amanda P Henry

doi:10.14814/phy2.13508

Bo Liu, Charlotte K Billington + Show 5 more

Open Access

https://doi.org/10.14814/phy2.13508

Copy DOI

Journal: Physiological reports	Publication Date: Jan 1, 2018
Citations: 12	License type: cc-by

Affiliation: University of Nottingham

Abstract

Chloride channels are known to play critical physiological roles in many cell types. Here, we describe the expression of anion channels using RNA Seq in primary cultures of human bronchial epithelial cells (hBECs). Chloride intracellular channel (CLIC) family members were the most abundant chloride channel transcripts, and CLIC1 showed the highest level of expression. In addition, we characterize the chloride currents in hBECs and determine how inhibition of CLIC1 via pharmacological and molecular approaches impacts these. We demonstrate that CLIC1 is able to modulate cyclic AMP‐induced chloride currents and suggest that CLIC1 modulation could be important for chloride homeostasis in this cell type.

Highlights

Chloride (ClÀ) channels are critically important in many physiological processes including muscle contraction, neuronal excitation, cell-volume regulation, transepithelial fluid transportation, acidification of intracellular organelles, and mucus production and secretion (Edwards and Kahl 2010)
CF is caused by mutations of the cystic fibrosis transmembrane conductance regulator (CFTR), a cyclic AMP-activated ClÀ channel expressed in the apical membrane of epithelial cells in airways, intestine, pancreas, testis, sweat ducts, and other fluid transporting tissues (Haq et al 2016)
Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society

Summary

Introduction

Chloride (ClÀ) channels are critically important in many physiological processes including muscle contraction, neuronal excitation, cell-volume regulation, transepithelial fluid transportation, acidification of intracellular organelles, and mucus production and secretion (Edwards and Kahl 2010). Dysfunction of ClÀ channels has been implicated in many diseases including osteoporosis, epilepsy, and myotonia with one of the most intensively investigated diseases being cystic fibrosis (CF) (Verkman 2009). CF is caused by mutations of the cystic fibrosis transmembrane conductance regulator (CFTR), a cyclic AMP (cAMP)-activated ClÀ channel expressed in the apical membrane of epithelial cells in airways, intestine, pancreas, testis, sweat ducts, and other fluid transporting tissues (Haq et al 2016). Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.

Objectives

Methods

Results