ArticleJournal of orthopaedic surgery and research2025
miR-302a-3p mitigates intervertebral disc degeneration progression through regulating EPHA2.
Article in Journal of orthopaedic surgery and research, 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.
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5 authors.
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Abstract
backgroundIntervertebral disc degeneration (IDD) underlying molecular mechanisms remain incompletely understood.
objectivesTo explore the role of miR-302a-3p in IDD and elucidate its targeted regulatory mechanism.
methods130 IDD patients and 130 healthy controls were collected. The miR-302a-3p and EPHA2 expressions were measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR). A lipopolysaccharide (LPS)-induced cell injury model was established using human nucleus pulposus (NP) cells. Proliferation was assessed using the cell counting kit-8 (CCK-8) assay, apoptosis was determined by flow cytometry, and the concentrations of inflammatory factors were measured by enzyme-linked immunosorbent assay (ELISA). A dual-luciferase reporter gene assay was conducted to confirm the targeted regulatory interaction.
resultsmiR-302a-3p expression was significantly decreased in IDD patients (P < 0.001), and receiver operating characteristic (ROC) curve analysis indicated that it possessed certain diagnostic potential (P < 0.001, AUC = 0.8808, 95% confidence interval (CI) = 0.8400-0.9216). In the LPS-induced NP cell injury model, miR-302a-3p expression was down-regulated, which was accompanied by reduced cell proliferation, increased apoptosis, and elevated tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) secretion (P < 0.001). However, overexpression of miR-302a-3p could effectively alleviate these injury-related effects. Furthermore, miR-302a-3p directly targeted EPHA2, whose expression was up-regulated in IDD (P < 0.001). Overexpression of EPHA2 partially reversed the protective effects of miR-302a-3p on cell proliferation, apoptosis, and inflammatory responses (P < 0.001).
conclusionmiR-302a-3p significantly mitigated inflammatory responses and suppressed cell apoptosis by directly targeting and downregulating EPHA2 expression, thereby delaying the progression of IDD.
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