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

Walailak Jantarajit1, Kannikar Wongdee2, Kornkamon Lertsuwan3

  • 1Center of Calcium and Bone Research (COCAB), Faculty of Science, Mahidol University, Bangkok, Thailand; Department of Physiology, Faculty of Science, Mahidol University, Bangkok, Thailand; School of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, UK.

Biochemical and Biophysical Research Communications
|January 20, 2020
PubMed
Summary

Parathyroid hormone (PTH) boosts anion secretion in intestinal cells by enhancing cystic fibrosis transmembrane conductance regulator (CFTR) function and increasing membrane surface area. This involves activating intermediate-conductance Ca2+-activated K+ channels (IKCa).

Keywords:
Cystic fibrosis transmembrane conductance regulator (CFTR)Intermediate-conductance Ca(2+)-activated K(+) channel (IKCa)Ion secretionParathyroid hormone (PTH)Patch-clamp technique

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Area of Science:

  • Cellular Physiology
  • Ion Transport Mechanisms
  • Gastrointestinal Biology

Background:

  • Parathyroid hormone (PTH) is known to influence various cellular processes.
  • Cystic fibrosis transmembrane conductance regulator (CFTR) plays a crucial role in anion secretion in epithelial cells.
  • The intestinal epithelial cell line Caco-2 is a widely used model for studying intestinal transport.

Purpose of the Study:

  • To investigate the mechanisms by which PTH stimulates CFTR-mediated anion secretion in Caco-2 cells.
  • To elucidate the role of membrane capacitance and specific ion channels in PTH-induced secretion.

Main Methods:

  • Patch-clamp electrophysiology to record ion channel activity.
  • Ussing chamber technique with impedance analysis to measure transepithelial ion transport and membrane capacitance.
  • Ion substitution experiments and pharmacological inhibitors (clotrimazole, TRAM-34, acetazolamide) to identify ion dependence and channel involvement.

Main Results:

  • PTH stimulated the opening of CFTR-like channels and increased apical membrane capacitance in Caco-2 cells.
  • PTH-stimulated short-circuit current (Isc) was dependent on chloride (Cl-) and bicarbonate (HCO3-) but not affected by carbonic anhydrase inhibition.
  • Clotrimazole, an intermediate-conductance Ca2+-activated K+ channel (IKCa) inhibitor, partially blocked PTH-stimulated Isc, while TRAM-34 did not directly inhibit CFTR.

Conclusions:

  • PTH enhances CFTR-mediated anion secretion in Caco-2 cells.
  • This enhancement involves increased CFTR expression/function in the apical membrane and activation of basolateral IKCa channels.
  • PTH's effects on intestinal anion secretion are complex, involving both CFTR and IKCa pathways.