ArticleRegenerative therapy2026
Effects and mechanisms of synovial mesenchymal stem cell-derived extracellular vesicular LncRNA-SNHG14 on chondrocyte injury.
Article in Regenerative therapy, 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
Objective: To investigate the effect of synovial mesenchymal stem cell (SMSC) derived extracellular vesicles (EVs) long non-coding ribonucleic acid (LncRNA) nuclear small RNA host gene 14 (SNHG14) on chondrocyte injury and its potential mechanism. Methods: EVs of SMSC were isolated and identified by transmission electron microscopy, nanoparticle tracking analysis, Western blot and EVs uptake test. Chondrocytes induced by interleukin-1β (IL-1β) were treated with EVs isolated from SMSCs transfected with sh-NC or sh-SNHG14. The proliferation and apoptosis of rat chondrocytes were detected by CCK-8 test and flow cytometry. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and insulin-like growth factor-1 (IGF-1) were detected by ELISA. Western blot was used to detect the expression of apoptosis-related proteins [Bcl-2-related X protein (Bax), cysteine aspartate protease-3 (caspase-3), cytochrome C (Cyt Results: LncRNA-SNHG14 in SMSC could be enriched and secreted in EVs, and chondrocytes can successfully uptake EVs. The expression level of LncRNA-SNHG14 in rat chondrocytes induced by IL-1β was increased, the cell survival rate was decreased, the apoptosis rate, TNF-α, IL-6 levels and Bax, caspase-3, Cytc, MMP-13 protein levels were increased, IGF-1 level and SOX9, COL2A1, bFGF protein levels were decreased, HMGB1, TLR4, NF-κB mRNA and protein levels were increased ( Conclusion: SMSC-EVs silencing LncRNA-SNHG14 can promote chondrocyte proliferation, inhibit chondrocyte apoptosis and inflammatory response in an in vitro model of IL-1β-induced chondrocyte injury. These effects are associated with reduced expression of HMGB1/TLR4/NF-κB pathway components, suggesting the involvement of this pathway.
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