Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of spinal cords from B10.PL mice with severe (stage 2.5-3) experimental autoimmune encephalomyelitis treated with placebo or 1,25-dihydroxyvitamin D3 to study the molecular mechanism of the compound.

ABSTRACT: B10.PL mice with severe (stage 2.5-3) experimental autoimmune encephalomyelitis were treated with placebo or 200 ng 1,25(OH)2D3. Six hours later, the spinal cords were harvested and mRNA was extracted for microarray analysis. Naive mice serve as controls. Individual samples were hybridized to individual microarrays.

ORGANISM(S): Mus musculus

DISEASE(S): reference

SUBMITTER: Karen Marie Spach

PROVIDER: E-GEOD-842 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Gene expression analysis suggests that 1,25-dihydroxyvitamin D3 reverses experimental autoimmune encephalomyelitis by stimulating inflammatory cell apoptosis.

Spach Karen M KM Pedersen Laura B LB Nashold Faye E FE Kayo Tsuyoshi T Yandell Brian S BS Prolla Tomas A TA Hayes Colleen E CE

Physiological genomics 20040708 2

Multiple sclerosis (MS) is a debilitating autoimmune disease of the central nervous system (CNS) that develops in genetically susceptible individuals who are exposed to undefined environmental risk factors. Epidemiological, genetic, and biological evidence suggests that insufficient vitamin D may be an MS risk factor. However, little is known about how vitamin D might be protective in MS. We hypothesized that 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] might regulate gene expression patterns in a ma ...[more]

PMID: 15138306

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Project description:The biological effects of 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) on osteoblast differentiation and function differ significantly depending upon the cellular state of maturation. To explore this phenomenon mechanistically, we examined the impact of 1,25(OH)2D3 on the transcriptomes of both pre-osteoblastic (POBs) and differentiated osteoblastic (OBs) MC3T3-E1 cells, and assessed localization of the vitamin D receptor (VDR) at sites of action on a genome-scale using ChIP-seq analysis. We observed that the 1,25(OH)2D3-induced transcriptomes of POBs and OBs were quantitatively and qualitatively different, supporting not only the altered biology observed but the potential for a change in VDR interaction at the genome as well. This idea was confirmed through discovery that VDR cistromes in POBs and OBs were also strikingly different. Depletion of VDR binding sites in OBs, due in part to reduced VDR expression, was the likely cause of the loss of VDR-target gene interaction. Continued novel regulation by 1,25(OH)2D3, however, suggested that factors in addition to the VDR might also be involved. Accordingly, we show that transcriptomic modifications are also accompanied by changes in genome binding of the master osteoblast regulator RUNX2 and the chromatin remodeler C/EBPβ. Importantly, genome occupancy was also highlighted by the presence of epigenetic enhancer signatures which were selectively changed in response to both differentiation and 1,25(OH)2D3. The impact of VDR, RUNX2, and C/EBPβ on osteoblast differentiation is exemplified by their actions at the Runx2 and Sp7 gene loci. We conclude that each of these mechanisms may contribute to the diverse actions of 1,25(OH)2D3 on differentiating osteoblasts. RNA was isolated and applied to gene expression microarrays in undifferentiated MC3T3-E1 cells as well as post 15 day osteogenic differentiation MC3T3-E1 cells, which were treated for 24 hours with 10-7M 1,25(OH)2D3. For the vehicle matched samples, please refer to study GSE41955. The samples were completed in biological triplicate.

Dataset Information

Transcription profiling of spinal cords from B10.PL mice with severe (stage 2.5-3) experimental autoimmune encephalomyelitis treated with placebo or 1,25-dihydroxyvitamin D3 to study the molecular mechanism of the compound.

Publications

Gene expression analysis suggests that 1,25-dihydroxyvitamin D3 reverses experimental autoimmune encephalomyelitis by stimulating inflammatory cell apoptosis.

Similar Datasets

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