Reference : RvD1(n-3 DPA) Downregulates the Transcription of Pro-Inflammatory Genes in Oral Epith...
Scientific journals : Article
Life sciences : Multidisciplinary, general & others
Human health sciences : Multidisciplinary, general & others
Systems Biomedicine
RvD1(n-3 DPA) Downregulates the Transcription of Pro-Inflammatory Genes in Oral Epithelial Cells and Reverses Nuclear Translocation of Transcription Factor p65 after TNF-α Stimulation.
Balta, Maria G. [> >]
Schreurs, Olav [> >]
Halder, Rashi [University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > Scientific Central Services]
Küntziger, Thomas M. [> >]
Saetre, Frank [> >]
Blix, Inger Johanne S. [> >]
Baekkevold, Espen S. [> >]
Glaab, Enrico mailto [University of Luxembourg > Luxembourg Centre for Systems Biomedicine (LCSB) > Biomedical Data Science]
Schenck, Karl [> >]
International journal of molecular sciences
[en] Humans ; Transcription Factor RelA/genetics/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; NF-kappa B/metabolism ; Active Transport, Cell Nucleus ; Inflammation/genetics/metabolism ; Epithelial Cells/metabolism ; NF-κB ; gingival ; oral epithelium ; oral inflammation ; p65 ; periodontitis ; resolvin ; specialized pro-resolving mediators
[en] Specialized pro-resolving mediators (SPMs) are multifunctional lipid mediators that participate in the resolution of inflammation. We have recently described that oral epithelial cells (OECs) express receptors of the SPM resolvin RvD1(n-3 DPA) and that cultured OECs respond to RvD1(n-3 DPA) addition by intracellular calcium release, nuclear receptor translocation and transcription of genes coding for antimicrobial peptides. The aim of the present study was to assess the functional outcome of RvD1(n-3 DPA)-signaling in OECs under inflammatory conditions. To this end, we performed transcriptomic analyses of TNF-α-stimulated cells that were subsequently treated with RvD1(n-3 DPA) and found significant downregulation of pro-inflammatory nuclear factor kappa B (NF-κB) target genes. Further bioinformatics analyses showed that RvD1(n-3 DPA) inhibited the expression of several genes involved in the NF-κB activation pathway. Confocal microscopy revealed that addition of RvD1(n-3 DPA) to OECs reversed TNF-α-induced nuclear translocation of NF-κB p65. Co-treatment of the cells with the exportin 1 inhibitor leptomycin B indicated that RvD1(n-3 DPA) increases nuclear export of p65. Taken together, our observations suggest that SPMs also have the potential to be used as a therapeutic aid when inflammation is established.
Luxembourg Centre for Systems Biomedicine (LCSB): Biomedical Data Science (Glaab Group)
Researchers ; Professionals ; Students
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