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. 2025 Feb;47(2):183-195.
doi: 10.1007/s13258-024-01598-4. Epub 2024 Nov 20.

miR-214-3p inhibits LPS-induced macrophage inflammation and attenuates the progression of dry eye syndrome by regulating ferroptosis in cells

Dandan Zhao #  1 , Hao Ji #  2 , Weijia Zhang  1 , Anni He  3 , Caizhe Guo  3 , Li Ma  3 , Yan Liu  4
Affiliations

miR-214-3p inhibits LPS-induced macrophage inflammation and attenuates the progression of dry eye syndrome by regulating ferroptosis in cells

Dandan Zhao et al. Genes Genomics. 2025 Feb.

Abstract

Background: Dry eye disease (DED) is an ocular illness caused by insufficient tear secretion or poor tear quality, and inflammation is a key factor in its pathogenesis. Previous studies have shown that miRNAs are important regulatory factors in DED.

Objective: The purpose of this study was to explore the potential mechanism by which miR-214-3p influenced the DED process by regulating the macrophage inflammatory response.

Methods: We induced THP-1 cells to differentiate into M0 macrophages with 100 ng/mL phorbol-12-myristate-13-acetate (PMA) and then added 15 ng/mL lipopolysaccharide (LPS) to induce inflammation. The expression of related genes and proteins was detected via RT‒qPCR, Western blotting, ELISA and immunofluorescence staining; cell viability was measured using the CCK-8 assay; and flow cytometry was used to detect ROS levels.

Results: In tear and serum samples from DED patients, the levels of miR-214-3p, IL-10, and Arg1 were decreased, and the levels of IL-6, TNF-α, IL-1β, and iNOS expression were increased. Moreover, the overexpression of miR-214-3p attenuated the effect of LPS and inhibited M1 polarization and inflammation in macrophages. Mechanistically, miR-214-3p inhibited macrophage ferroptosis by downregulating TFRC expression, thereby inhibiting macrophage M1 polarization and inflammation and alleviating the progression of DED.

Conclusions: Our study indicated that the upregulation of miR-214-3p expression might be a new target for DED therapy.

Keywords: Dry eye syndrome; Ferroptosis; Inflammation; Macrophages; TFRC; miR-214-3p.

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: Informed consent was obtained from all of the patients. The experiments were approved by the Medical Ethics Committee of Yan ‘an Hospital of Kunming City (approval number: 2022-056-01), and all of the methods/studies were conducted in accordance with the Declaration of Helsinki. Competing interests: The authors declare that they have no competing interests.

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