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Parathyroid hormone increases CFTR expression and function in Caco-2 intestinal epithelial cells.

Abstract：

: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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Jantarajit W,Wongdee K,Lertsuwan K,Teerapornpuntakit J,Aeimlapa R,Thongbunchoo J,Harvey BSJ,Sheppard DN,Charoenphandhu N

doi

10.1016/j.bbrc.2019.12.106

subject

Has Abstract

pub_date

2020-03-12 00:00:00

pages

816-821

issue

3

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(20)30057-7

journal_volume

523

pub_type

杂志文章

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