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KCNQ gene expression and functional role in H441 epithelial cells
Author(s) -
Yeung Shuk Yin,
Hettiarachi Samila,
Baines Debbie,
Greenwood Iain
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a545-c
Subject(s) - transcellular , microbiology and biotechnology , potassium channel , chemistry , amiloride , charybdotoxin , epithelial sodium channel , potassium channel blocker , channel blocker , biophysics , biology , sodium , organic chemistry , calcium
Potassium (K) channels regulate transcellular sodium flux in airway epithelia by providing a membrane potential for Na movement. The aim of this study was to determine if K channels encoded by KCNQ genes were expressed in polarized human bronchial epithelial cells (H441) and whether they influence Na flux as determined by the sensitivity to amiloride. Short circuit current (I SC ) across H441 monolayers were measured using Ussing chambers. Application of the KCNQ channel blocker XE991 (1–100 μM) to the apical side provided a marked reduction in I SC and also decreased the amplitude of the amiloride‐sensitive current. Xe991 applied to the basolateral side also reduced I SC but to a lesser extent than when applied apically. Chromanol 293B (30 μM) a blocker of cardiac delayed rectifiers comprised of KCNQ1 in association with KCNE1 expression products also affected I SC . RT‐PCR experiments revealed that KCNQ3 and Q5 were abundantly expressed in H441 cells with Q1 and Q4 at lower levels and Q2 not expressed. These data show for the first time the presence of KCNQ genes, considered to be specifically expressed in neurones, in human epithelia and highlights a functional role for the products of these genes in determining Na flux. This work was supported by the British Heart Foundation.