Clinical Cohort Analysis of miR-215-5p as a Diagnostic Biomarker for Osteoarthritis and its Mechanism via EREG in IL-1β-Induced Chondrocyte Model.

Authors

Dejian Yang, Lihua Gong, Xiong Chen, Zhiwei Zeng

Published in

Journal of visualized experiments : JoVE. Issue 233. Jul 31, 2026. Epub Jul 31, 2026.

Abstract

Osteoarthritis (OA) is a degenerative joint disease marked by degradation of joint cartilage and synovial inflammatory infiltration. This study aims to evaluate serum miR-215-5p as a diagnostic biomarker for OA and to investigate its regulatory mechanism in IL-1β-induced chondrocytes. 110 OA patients and 105 healthy controls were recruited. Serum miR-215-5p and EREG expression were determined by quantitative reverse transcription polymerase chain reaction. The diagnostic value of miR-215-5p for OA was assessed using a receiver operating characteristic curve. C28/I2 chondrocytes were stimulated with IL‑1β to construct an OA cell model. Cell viability, migration ability, and inflammatory cytokine levels were evaluated via Cell Counting Kit-8, Transwell assay, and an enzyme-linked immunosorbent assay (ELISA). The association between miR-215-5p and EREG was validated using a dual-luciferase reporter assay and an RNA immunoprecipitation (RIP) assay. In OA patients, serum miR-215-5p was upregulated, while EREG was downregulated. MiR-215-5p exhibited good diagnostic performance for OA (area under the curve, AUC = 0.883). In interleukin-1β (IL-1β)-treated C28/I2 cells, inhibition of miR-215-5p enhanced cell viability and migration, and attenuated IL-1β, IL-6, and tumor necrosis factor-α (TNF-α) levels. EREG was confirmed to be a direct target of miR-215-5p. Knockdown of EREG partially reversed the promoting effect of miR-215-5p downregulation on the viability and migration capacity of IL-1β-treated C28/I2 cells and attenuated its inhibitory effect on inflammatory factors. miR-215-5p contributes to OA pathogenesis by regulating EREG and represents a promising diagnostic biomarker and potential therapeutic target for OA.

PMID:
42612080
Bibliographic data and abstract were imported from PubMed on 19 Aug 2026.

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