ArticleMolecular biology reports2025
Epigenetic regulation of TIMP-3 expression in human macrophages via physiological and pharmacological modification of histone3 lysine27 (H3K27).
Article in Molecular biology reports, 2025. 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
backgroundTissue inhibitor of metalloproteinases-3 (TIMP-3) prevents over-activity of metalloproteinases, thereby reducing the severity of several immune/ inflammatory diseases in which T-lymphocyte-stimulated macrophage invasion plays an essential role. However, the underlying mechanism of TIMP-3 expression and its modulation by anti-inflammatory agents are poorly understood. METHODS AND
resultsUsing RT-qPCR measurements in human macrophages, we showed that TIMP-3 steady-state and pre-spliced mRNAs are induced by the Thelper2 cytokine, interleukin-4 (IL-4) but downregulated by the pro-inflammatory Thelper1 cytokine, interferon-γ (IFN-γ), an inhibitory effect confirmed at the protein level. These effects of IL-4 and IFN-γ were independent of changes in the lineage determining transcription factors, CEBP-β, SP-1 and PU1/ETS, suggesting that epigenetic regulation might be important. We investigated the action of GSK-J4, an inhibitor of the histone3 lysine27 (H3K27) demethylase (KDM6) enzymes. GSK-J4 decreased basal and IL-4 induced TIMP-3 levels, concomitant with increased H3K27 tri-methylation (H3K27me
conclusionsIn conclusion GSK-J4 reduces TIMP-3 expression and might therefore paradoxically increase macrophage invasion. By contrast, the HDAC inhibitor MS-275 antagonised the depression of TIMP-3 expression by IFN-γ, which should reduce macrophage invasion.
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