ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Generation and functional characterization of epithelial cells with stable expression of SLC26A9 Cl- channels.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- Nucleotide Variant in theJournal of clinical medicine · 2026Article
- Human induced pluripotent stem cells for in vitro modeling of impaired mucociliary clearance in cystic fibrosis lung disease.Stem cell research & therapy · 2025Article
- Molecular mechanism underlying phosphate distribution by SULTR family transporter SPDT inScience advances · 2025Article
- The role of the STAS domain in SLC26A9 for chloride ion transporter function.Biophysical journal · 2024Article
- Pathogenic Relationships in Cystic Fibrosis and Renal Diseases: CFTR, SLC26A9 and Anoctamins.International journal of molecular sciences · 2023Review
- Drug Repurposing for Cystic Fibrosis: Identification of Drugs That Induce CFTR-Independent Fluid Secretion in Nasal Organoids.International journal of molecular sciences · 2022Article
- SLC26A9 deficiency causes gastric intraepithelial neoplasia in mice and aggressive gastric cancer in humans.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Genetic evidence supports the development of SLC26A9 targeting therapies for the treatment of lung disease.NPJ genomic medicine · 2022Article
- Expression of SLC26A9 in Airways and Its Potential Role in Asthma.International journal of molecular sciences · 2022Article
- SLC26A9 as a Potential Modifier and Therapeutic Target in Cystic Fibrosis Lung Disease.Biomolecules · 2022Review
- Age-Related Differences in Structure and Function of Nasal Epithelial Cultures From Healthy Children and Elderly People.Frontiers in immunology · 2022Article
- SLC26A9 is selected for endoplasmic reticulum associated degradation (ERAD) via Hsp70-dependent targeting of the soluble STAS domain.The Biochemical journal · 2021Article
- Separating the contributions of SLC26A9 and CFTR to anion secretion in primary human bronchial epithelia.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Airway Surface Liquid pH Regulation in Airway Epithelium Current Understandings and Gaps in Knowledge.International journal of molecular sciences · 2021Review
- A Peptide-Nucleic Acid Targeting miR-335-5p Enhances Expression of Cystic Fibrosis Transmembrane Conductance Regulator (Biomedicines · 2021Article
- Pharmacological Modulation of Ion Channels for the Treatment of Cystic Fibrosis.Journal of experimental pharmacology · 2021Review
- Increased expression of anion transporter SLC26A9 delays diabetes onset in cystic fibrosis.The Journal of clinical investigation · 2020Article
- Structural insights into the gating mechanism of human SLC26A9 mediated by its C-terminal sequence.Cell discovery · 2020Article
- Emerging Concepts and Therapies for Mucoobstructive Lung Disease.Annals of the American Thoracic Society · 2018Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Recent studies identified the SLC26A9 Cl(-) channel as a modifier and potential therapeutic target in cystic fibrosis (CF). However, understanding of the regulation of SLC26A9 in epithelia remains limited and cellular models with stable expression for biochemical and functional studies are missing. We, therefore, generated Fisher rat thyroid (FRT) epithelial cells with stable expression of HA-tagged SLC26A9 via retroviral transfection and characterized SLC26A9 expression and function using Western blotting, immunolocalization, whole cell patch-clamp, and transepithelial bioelectric studies in Ussing chambers. We demonstrate stable expression of SLC26A9 in transfected FRT (SLC26A9-FRT) cells on the mRNA and protein level. Immunolocalization and Western blotting detected SLC26A9 in different intracellular compartments and to a lesser extent at the cell surface. Whole cell patch-clamp recordings demonstrated significantly increased constitutive Cl(-) currents in SLC26A9-FRT compared with control-transduced FRT (Control-FRT) cells (P < 0.01). Similar, transepithelial measurements showed that the basal short circuit current was significantly increased in SLC26A9-FRT vs. Control-FRT cell monolayers (P < 0.01). SLC26A9-mediated Cl(-) currents were increased by cAMP-dependent stimulation (IBMX and forskolin) and inhibited by GlyH-101, niflumic acid, DIDS, and 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB), as well as RNAi knockdown of WNK1 implicated in epithelial osmoregulation. Our results support that these novel epithelial cells with stable expression of SLC26A9 will be a useful model for studies of pharmacological regulation including the identification of activators of SLC26A9 Cl(-) channels that may compensate deficient cystic fibrosis transmembrane regulator (CFTR)-mediated Cl(-) secretion and serve as an alternative therapeutic target in patients with CF and potentially other muco-obstructive lung diseases.
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