ArticleJournal of orthopaedic surgery and research2026
Long non-coding RNA LINC-PINT: emerging clinical significance and molecular mechanisms in knee osteoarthritis.
Article in Journal of orthopaedic surgery and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe underlying pathophysiological mechanisms of knee osteoarthritis (KOA) remain incompletely understood. This study aimed to investigate the clinical significance of long non-coding RNA LINC-PINT in KOA and elucidate its molecular mechanism in regulating chondrocyte function via the miR-324-3p/GPX4 axis.
methods100 KOA patient samples and 40 normal knee cartilage tissue samples were collected, and the relevant gene expression was quantified using RT-qPCR. C28/I2 was cultured in vitro to establish an IL-1β-induced KOA cellular model. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to validate the targeted molecular regulatory interactions. Cell proliferation and apoptosis, as well as inflammatory factors levels, were assessed using cell counting kit-8 (CCK-8), flow cytometry, and enzyme-linked immunosorbent assay (ELISA), respectively. Oxidative stress-related indicators and Fe
resultsIn KOA tissues, LINC-PINT and glutathione peroxidase 4 (GPX4) were significantly downregulated, whereas miR-324-3p was markedly upregulated. LINC-PINT demonstrated the potential diagnostic discrimination ability and was identified as an independent protective factor in KOA. Overexpression of LINC-PINT effectively counteracted interleukin-1 beta (IL-1β)-induced suppression of chondrocyte proliferation, reduced apoptosis, and attenuated the secretion of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), while significantly alleviating cartilage matrix degradation, as indicated by increased expression of collagen II and aggrecan and decreased matrix metallopeptidase 13 (MMP13) levels. Moreover, LINC-PINT directly bound to miR-324-3p, which in turn directly targeted GPX4. Functional rescue assays further confirmed that transfection with a miR-324-3p mimic reversed the protective effects of LINC-PINT overexpression on chondrocytes, whereas GPX4 overexpression mitigated the detrimental effects induced by the miR-324-3p mimic. IL-1β disrupted the cellular redox balance by increasing the levels of Fe
conclusionLINC-PINT demonstrated the potential diagnostic discrimination ability and exerted a protective effect in KOA by modulating the miR-324-3p/GPX4 axis.
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