Unknown,Transcriptomics,Genomics,Proteomics

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IL-36R stimulation of colonic mouse fibroblasts

ABSTRACT: Intestinal fibroblasts from the colons of C57BL/6 wild-type mice were grown in the presence or absence of IL-36ÉŁ (30 ng/ml) for 4 hours. The experimental setup included 6 samples from 3 colons in a pairwise design (3 stimulated vs 3 unstimulated). Profiling of whole-genome transcriptomic patterns was performed with 1.2 Âľg high quality total RNA per sample by RNA-seq at the Next Generation Sequencing core unit of the university hospital Erlangen. The sequencing platform was Illumina HiSeq-2500 with high output mode and single-end 100bp fragments. The sequencing library was NuGEN Ovation RNA-Seq Library Prep-Kit. Demultiplexed reads were corrected regarding rRNAs, tRNAs, mt-rRNAs and mt-tRNAs. Alignment against the mus musculus reference genome (Ensemble version 75 for GRCm38) was performed with RNAseq aligner STAR (version 2.4.0.i) and quantification (HTseq count) was done of unique mappings.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Clemens Neufert

PROVIDER: E-MTAB-3814 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:MUC1 is a tumor-associated antigen that is aberrantly expressed in cancer and inflammatory bowel disease (IBD). Even though immune cells express low MUC1 levels, their modulations of MUC1 are important in tumor progression. Consistent with previous clinical data that show increased myeloid-derived suppressor cells (MDSCs) in IBD, we now show that down-regulation of MUC1 on hematopoietic cells increases MDSCs in IBD, similar to our data in tumor-bearing mice. We hypothesize that MDSC expansion in IBD is critical for tumor progression. In order to mechanistically confirm the linkage between Muc1 down-regulation and MDSC expansion, we generated chimeric mice that did not express Muc1 in the hematopoietic compartment (KOM-bM-^FM-^RWT). These mice were used in 2 models of colitis and colitis-associated cancer (CAC) and their responses were compared to wildtype chimeras (WTM-bM-^FM-^RWT). KOM-bM-^FM-^RWT mice show increased levels of MDSCs during colitis that was responsible for the larger colon tumors that eventually developed in these mice. Using microarray and qRT-PCR analysis, we observed increased pro-tumorigenic signaling in the colons of KOM-bM-^FM-^RWT mice during colitis as compared to WTM-bM-^FM-^RWT mice. Our RNA (microarray and qRT-PCR analysis) and protein analysis demonstrate increased up-regulation of metalloproteinases, collagenases, defensins, complements, growth factors, cytokines and chemokines in KOM-bM-^FM-^RWT mice as compared to WTM-bM-^FM-^RWT mice. Antibody-mediated depletion of MDSCs in mice during colitis reduced colon tumor formation during CAC. Development of CAC is a serious complication of colitis and our data highlight MDSCs as a targetable link between inflammation and cancer. A total of 12 samples were analysed. RNA was made from the mucosa of the colon of WTM-bM-^FM-^RWT and KOM-bM-^FM-^RWT mice that were either untreated or treated with azoxymethane (AOM) and dextran sodium sulfate (DSS). There are 4 groups, n=3 for each group: untreated WTM-bM-^FM-^RWT mice, untreated KOM-bM-^FM-^RWT mice, AOM+DSS treated WTM-bM-^FM-^RWT mice, AOM+DSS treated KOM-bM-^FM-^RWT mice = 12 samples in total.

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IL-36R stimulation of colonic mouse fibroblasts

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