ArticleMolecular biology reports2025
Epithelial sodium channel in dendritic cells participates in high-fat-induced inflammatory responses.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- BMI-Dependent Associations of the Estradiol-Linked Polymorphism rs117585797 of theLife (Basel, Switzerland) · 2026Article
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Abstract
BACKGROUND AND
objectiveTo investigate the role and mechanism of epithelial sodium channel (ENaC) in the inflammatory response of dendritic cells (DCs) induced by high fat, oxidized low-density lipoprotein (ox-LDL) was employed to trigger an inflammatory response in DCs.
methodDCs were cultured in vitro and induced with high fat using ox-LDL, with or without benzamil (a specific ENaC blocker). Changes in protein expression levels of ENaC, calcineurin (CaN), total nuclear factor of activated T-cells 1 (t-NFATc1) and phospho-NFATc1 (p-NFATc1) in DCs were determined by western blot. Changes in mRNA levels of inflammatory factors, matrix metalloproteinase 9 (MMP9), and tissue inhibitor of metalloproteinases 2 (TIMP2) in DCs were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR). Changes in intracellular [Ca²⁺] in DCs were detected using a calcium fluorescent probe.
resultsOx-LDL upregulated the protein expression levels of α-ENaC and γ-ENaC in DCs. Benzamil reduced the release of inflammatory factors in ox-LDL-induced DCs. Inhibition of ENaC significantly decreased the mRNA expression of MMP9 and increased TIMP2 in ox-LDL-induced DCs. Inhibition of ENaC significantly decreases the aberrant increase in [Ca²⁺] in ox-LDL-induced DCs, and also significantly decreases the increased protein expression levels of CaN and its downstream t-NFATc1, however, the protein level of p-NFATc1 was significantly elevated.
conclusionENaC in DCs critically mediates high-fat-induced inflammation. The mechanism may involve ox-LDL upregulating α-ENaC and γ-ENaC in DCs, leading to increased intracellular [Na⁺], which elevates intracellular [Ca²⁺] via Na+/Ca2+ exchanger (NCX). This subsequently triggers the inflammatory response through the Ca²⁺-CaN-NFATc1 signaling pathway. This research provides new evidence for the theoretical basis of immunotherapy for atherosclerosis (AS).
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