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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/49555
Title: Parathyroid hormone increases CFTR expression and function in Caco-2 intestinal epithelial cells
Authors: Walailak Jantarajit
Kannikar Wongdee
Kornkamon Lertsuwan
Jarinthorn Teerapornpuntakit
Ratchaneevan Aeimlapa
Jirawan Thongbunchoo
Bartholomew S.J. Harvey
David N. Sheppard
Narattaphol Charoenphandhu
Naresuan University
University of Bristol
Mahidol University
Burapha University
Academy of Science
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 1-Jan-2020
Citation: Biochemical and Biophysical Research Communications. (2020)
Abstract: © 2020 Elsevier Inc. Parathyroid hormone (PTH) enhances cystic fibrosis transmembrane conductance regulator (CFTR)-mediated anion secretion by the human intestinal epithelial cell line Caco-2. With the patch-clamp and Ussing chamber techniques, we investigated how PTH stimulates CFTR activity in Caco-2 cells. Cell-attached recordings revealed that PTH stimulated the opening of CFTR-like channels, while impedance analysis demonstrated that PTH increased apical membrane capacitance, a measure of membrane surface area. Using ion substitution experiments, the PTH-stimulated increase in short-circuit current (Isc), a measure of transepithelial ion transport, was demonstrated to be Cl−- and HCO3−-dependent. However, the PTH-stimulated increase in Isc was unaffected by the carbonic anhydrase inhibitor acetazolamide, but partially blocked by the intermediate-conductance Ca2+-activated K+ channel (IKCa) inhibitor clotrimazole. TRAM-34, a related IKCa inhibitor, failed to directly inhibit CFTR Cl− channels in cell-free membrane patches, excluding its action on CFTR. In conclusion, PTH enhances CFTR-mediated anion secretion by Caco-2 monolayers by increasing the expression and function of CFTR in the apical membrane and IKCa activity in the basolateral membrane.
URI: http://repository.li.mahidol.ac.th/dspace/handle/123456789/49555
metadata.dc.identifier.url: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85077922389&origin=inward
ISSN: 10902104
0006291X
Appears in Collections:Scopus 2020

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