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Updated: Jul 15, 2026

A Fluorescence-Based Assay of Membrane Potential for High-Throughput Functional Study of Two Endogenous Ion Channels in Two Epithelial Cell Lines
Published on: June 22, 2022
SLC26A7 can function as a chloride-loading mechanism in parietal cells
Ortrud Kosiek1, Stephanie M Busque, Michael Föller
1Department of Surgery, Yale University School of Medicine, BML 265, 310 Cedar Street, New Haven, CT, 06520, USA.
The SLC26A7 protein facilitates chloride (Cl-) entry into parietal cells, crucial for acid secretion. This study identifies SLC26A7 as a key pathway for histamine-stimulated acid production in the stomach.
Area of Science:
- Physiology
- Cell Biology
- Gastroenterology
Background:
- Parietal cells secrete gastric acid, a process requiring basolateral chloride (Cl-) entry.
- Potential Cl- entry pathways include AE2, SLC26A7, and NKCC1.
Purpose of the Study:
- To investigate the contribution of AE2, SLC26A7, and NKCC1 to secretagogue-stimulated acid secretion in rat gastric parietal cells.
Main Methods:
- Microfluorimetry to monitor Cl- influx and intracellular pH (pH(i)) changes.
- Pharmacological inhibition and ion manipulation to assess transporter activity.
- Immunohistochemistry and Western blot to confirm SLC26A7 expression.
Main Results:
- Histamine stimulation enhanced Cl- influx, dependent on Na+ and endogenous HCO(3)-.
- A low and high 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS)-sensitive HCO(3)- extrusion system contributed to Cl- uptake.
- Acidic pH(i) and H+,K+-ATPase activity were abolished by 5-Nitro-2-(3-phenylpropyl-amino)benzoic acid (NPPB) and high DIDS, but not bumetanide.
- SLC26A7 was identified as a Cl- uptake system under histamine stimulation.
Conclusions:
- SLC26A7 plays a significant role in mediating Cl- uptake during histamine-stimulated acid secretion.
- The findings elucidate the molecular mechanisms of Cl- transport in gastric acid production.
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