ArticleJournal of inflammation (London, England)2026
TCF4 contributes to OA progression by regulating the transcription of LOXL1.
Article in Journal of inflammation (London, England), 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
backgroundOsteoarthritis (OA) is a chronic degenerative joint disease that seriously affects patients’ quality of life. Lysyl oxidase like 1 (LOXL1), a member of the lysyl oxidase protein family, whose role in OA is unknown.
methodsThe gene expression pattern was investigated by the Gene Expression Omnibus database. Quantitative real-time PCR (qRT-PCR) and western blot were used to detect the gene expression in tissues and cells. Interleukin-1β (IL-1β) was applied to induce an inflammatory chondrocyte injury model in vitro, mimicking certain aspects of OA pathology, and the cell viability was measured by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl tetrazolium bromide (MTT) assay. 5-Ethynyl-2’-deoxyuridine (EdU) staining, flow cytometry, and enzyme linked immunosorbent assay (ELISA) assays were utilized for function examination. In addition, the monoiodoacetate (MIA)-induced arthritis mouse models were constructed to evaluate the effects of LOXL1 in vivo, and the hematoxylin-eosin (H&E) staining, safranin-O/fast green (SOFG) staining, and immunohistochemistry (IHC) were used to estimate the histological and morphological changes of the knee joints obtained from the mice. The transcriptional binding between genes was verified by chromatin immunoprecipitation (ChIP) and dual luciferase reporter assay.
resultsLOXL1 was up-regulated in tissues of OA. The down-regulation of LOXL1 promoted cell proliferation and inhibited apoptosis, inflammation, oxidative stress, and extracellular matrix (ECM) degradation in vitro. Meanwhile, LOXL1 knockdown exhibited the same results in vivo. Mechanically, transcription factor 4 (TCF4) activated the transcription of LOXL1, and TCF4 deficiency-mediated effects on chondrocyte injury were weakened by LOXL1.
conclusionIn summary, TCF4 may contribute to OA pathology by activating LOXL1 transcription, and the TCF4/LOXL1 axis is involved in IL-1β-induced chondrocyte dysfunction and MIA-induced joint degeneration.
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