Publication: Parathyroid hormone increases CFTR expression and function in Caco-2 intestinal epithelial cells
Issued Date
2020-01-01
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ISSN
10902104
0006291X
0006291X
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2-s2.0-85077922389
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Mahidol University
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SCOPUS
Bibliographic Citation
Biochemical and Biophysical Research Communications. (2020)
Suggested Citation
Walailak Jantarajit, Kannikar Wongdee, Kornkamon Lertsuwan, Jarinthorn Teerapornpuntakit, Ratchaneevan Aeimlapa, Jirawan Thongbunchoo, Bartholomew S.J. Harvey, David N. Sheppard, Narattaphol Charoenphandhu Parathyroid hormone increases CFTR expression and function in Caco-2 intestinal epithelial cells. Biochemical and Biophysical Research Communications. (2020). doi:10.1016/j.bbrc.2019.12.106 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/49555
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Title
Parathyroid hormone increases CFTR expression and function in Caco-2 intestinal epithelial cells
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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.