Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA101331 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The ability of dendritic cells (DC) to initiate immunity and induce antigen-specific tolerance makes DC ideal targets for pharmacological intervention into immune responses. NF-kB factors are a family of transcriptional regulators important for DC development and function. However, the identity of NF-kB target genes that are central to DC biology is largely unknown. In the present study inhibition of the NF-kB activation by the IkBa super repressor (IkBa-SR) and DNA microarray analysis were used to determine the repertoire of NF-kB responsive genes in DC. A number of immunomodulatory compounds have been suggested to target the NF-kB signalling pathway and/or NF-kB-mediated transcription of pro-inflammatory target genes. 1a,25-dihydroxyvitamin D3 (VD3) exerts its effects through the vitamin D3 receptor (VDR), a member of the nuclear hormone receptor superfamily. Microarray analysis was also selected as an approach of choice for the analysis of the effects of VD3 on the activation of DC, and to survey the involvement of VDR in repression of NF-kB regulated genes. These genes can be potentially useful targets for the development of more specific anti-inflammatory agents for clinical applications. Keywords: drug treatment, TNFa treatment, VD3 treatment DC were generated in vitro from bone marrow cells of VDRmut and VDRwt control mice as described previously (Hieronymus, T., T. C. Gust, R. D. Kirsch, T. Jorgas, G. Blendinger, M. Goncharenko, K. Supplitt, S. Rose-John, A. M. Muller, and M. Zenke. 2005. Progressive and controlled development of mouse dendritic cells from Flt3+CD11b+ progenitors in vitro. J Immunol 174:2552-2562). Immature DC were pre-treated with 1a,25-dihydroxyvitamin D3 (VD3), or left untreated. TNFa was added where appropriate, and cells incubated further for 4 h. Total RNA was amplified, labelled and hybridised to Affymetrix MOE430A arrays. TNFa up- and down-regulated genes, as well as genes affected by VD3 were analysed.
2012-12-31 | E-GEOD-8334 | biostudies-arrayexpress
Project description:To investigate the expression of glycosyltransferases in dendritic cells and the changes in expression associated with maturation. RNA preparations from 5 different immature and mature dendritic cells subsets, with and without LPS from 2 different donors (20 different samples); (iDC, IL-10 iDC, Dexamethason iDC, Vitamin D3 iDC, im. macrophage), (mDC, IL-10 mDC, Dexamethason mDC, Vitamin D3 mDC, m. macrophage) were sent to both Microarray Core (E) and Core(C). The RNA was purified on an RNeasy Column, amplified, labeled, and hybridized to the Glycov3 microarrays.
2011-06-14 | E-GEOD-29944 | biostudies-arrayexpress
Project description:The ability of dendritic cells (DC) to initiate immunity and induce antigen-specific tolerance makes DC ideal targets for pharmacological intervention into immune responses. NF-kB factors are a family of transcriptional regulators important for DC development and function. However, the identity of NF-kB target genes that are central to DC biology is largely unknown. In the present study inhibition of the NF-kB activation by the IkBa super repressor (IkBa-SR) and DNA microarray analysis were used to determine the repertoire of NF-kB responsive genes in DC. A number of immunomodulatory compounds have been suggested to target the NF-kB signalling pathway and/or NF-kB-mediated transcription of pro-inflammatory target genes. 1a,25-dihydroxyvitamin D3 (VD3) exerts its effects through the vitamin D3 receptor (VDR), a member of the nuclear hormone receptor superfamily. Microarray analysis was also selected as an approach of choice for the analysis of the effects of VD3 on the activation of DC, and to survey the involvement of VDR in repression of NF-kB regulated genes. These genes can be potentially useful targets for the development of more specific anti-inflammatory agents for clinical applications. Keywords: drug treatment, TNFa treatment, VD3 treatment
2012-12-31 | GSE8334 | GEO
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Vitamin D deficiency is associated with a decline in muscle function and an increasing risk of muscle injury in athletes and the elderly. Nevertheless, how vitamin D3 and vitamin D receptor (VDR) regulate skeletal muscle cells under pro-fibrotic factor stimulation that could be pronounced during repetitive muscle damage have not been elucidated. Therefore, this study aimed to investigate the regulatory role of cholecalciferol (D3), calcidiol (25D3), calcitriol (1,25D3), and the effect of Vdr gene suppression under TGF-β1 stimulation in C2C12 mouse skeletal muscle cells. All forms of vitamin D3 exerted anti-fibrotic effects under TGF-β1 stimulation by suppression of COL1A1; however, D3 preserves this effect without a negative impact on myogenesis. Moreover, LC-MS/MS-based proteomics analysis revealed that myoblast fusion protein and mitochondrial regulation were altered following Vdr knockdown. These changes were associated with exacerbation of α-SMA expression in TGF-β1-treated cells and suggested VDR modulates fibrogenesis in skeletal muscle cells regardless of ligand binding. Under TGF-β1 stimulation, anti-fibrotic effects of 1,25D3 but not D3 were diminished after Vdr knockdown, supporting D3 action is not dependent on VDR activation. Collectively, understanding anti-fibrotic effects of vitamin D3 is beneficial for providing a strategy of vitamin D supplementation to counteract fibrosis development after muscle injury.
2025-12-01 | PXD062669 | Pride
Project description:We performed single-cell RNA sequencing on bone marrow derived, cultured dendritic cells after CRISPR-knockout of Ndrg2, after vitamin D3 treatment or no treatment. In addition we performed single-cell RNA sequencing of wounds that had been treated with hydrogels seeded with Ndrg2-KO dendritic cells, control (untreated) dendritic cells or blank hydrogels.
2023-06-09 | GSE234145 | GEO
Project description:Complex autoimmune diseases have proven difficult to dissect down to their causative genetic mechanisms. As a result, epidemiological data from different human association studies are often merged to arrive at a working hypothesis. In one of such examples, lack of sun exposure and consequent lower serum vitamin D3 levels has been proposed to increase risk of autoimmunity, attributing vitamin D3 an immune regulatory role. However, conclusive evidence demonstrating its efficacy in treating autoimmune diseases is missing. In this study, we have used a forward genetics approach to positionally identify polymorphic nucleotides controlling T cell-dependent inflammatory diseases using congenic mouse strains. Here, we identify the vitamin D3 receptor (Vdr) as a driver of inflammation. Congenic mice carrying a polymorphic Vdr allele overexpressed the receptor selectively in activated T cells, thereby escaping systemic calcaemic side effects that often constitute a confounding factor in the study of immunomodulation by vitamin D3. Mice overexpressing Vdr in T cells developed more severe collagen-induced arthritis (CIA) and exhibited an enhanced antigen-specific CD4+ T cell response. Deficiency of vitamin D3 completely protected mice from CIA by limiting the activation of antigen-specific T cell responses, and arthritis susceptibility was restored by re-administration of vitamin D3. We demonstrate that vitamin D3 signalling specifically through Vdr predominantly acts to enhance T cell proliferation, thereby contributing to inflammation. In conclusion, our results demonstrate that genetically determined expression of VDR codetermines the pro-inflammatory behaviour of activated T cells. Furthermore, our data suggest that the anti-inflammatory properties of vitamin D3 might be limited by high expression of VDR at the site of inflammation.
2020-09-28 | PXD019876 | Pride
Project description:This experiment is designed to compare the effects of Vitamin D3 treatment of mouse bone marrow derived dendritic cells with control, untreated cells, and additional effects of maturation of either treated or control cells with LPS.
2006-11-01 | E-MEXP-506 | biostudies-arrayexpress
Project description: Not available
| S-EPMC11335981 | biostudies-literature
Project description:The comparative analysis of the transcriptome of tolerogenic dendritic cells (tolDC) differentiated using different stimulus (either vitamin D3, dexamethasone or rapamycin) would allow to evidence potential common genes and pathways that could explain their potency as tolerance-inducing cells.
2018-07-31 | E-MTAB-6937 | biostudies-arrayexpress