RNA sequencing of Jejunum of WT and IL23 expression mice (KSR23)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA565405 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10116206.fastq.gz | Fastqsanger.gz | |||
| SRR10116207.fastq.gz | Fastqsanger.gz | |||
| SRR10116208.fastq.gz | Fastqsanger.gz | |||
| SRR10116209.fastq.gz | Fastqsanger.gz | |||
| SRR10116210.fastq.gz | Fastqsanger.gz |
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Project description:The goal of this study is to check if elevated level of IL-23 and/or its downstream cytokines affect the gene expression in the jejunum of newborn mice. We engineered a mice strain in which the expression of IL-23 was directed to the keratinocytes (KSR23). The KSR23 mice had normal body weight at birth and much smaller than their control littermates at day 5. KSR23 mice died prematurely (before 15 days of age), but displayed no signs of disease in the skin, intestine, or in other organs examined. To investigate if elevated level of IL-23 and/or its downstreamcytokines could affect body growth, we examined the transcriptome of the the intestine, which are critical for the processing and absorption of nutrients. Jejunum mRNA profiles of 5-day-old WT and KSR23 were generated by deep sequencing. The transcriptome of the Jejunum of KSR23 mice at P5 differed significantly from that of their control littermates (WT). Several genes were differentially expressed, including IL-22, and genes that are downstream of it such as Reg3 genes and digestive enzymes also produced by the jejunum. Kegg pathway analysis of WT and KSR23 jejunum indicated that genes involved in protein digestion and absorption such as chymotrypsinogen B1 (Ctrb1), trypsinogen (Prss1), trypsin (Tyr5 and Tyr4), caboxypeptidase a1 (Cpa1) and chymotrypsin-like elastase family member 3b (Cela3b), were downregulated in the intestine of KSR23 mice. Transcriptome analysis also showed decreased expression of several genes involved in the regulation of the very low-density lipoprotein particle pathway (VLDL). These particles regulate fat and cholesterol release into the bloodstream. Together, these results indicate that systemic expression of IL-23, and other cytokines, correlated with significant transcriptional changes in genes that regulate food processing in the intestine.
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Project description:Using mice deficient in hepatic cytochrome-P450 oxidoreductase (POR), which disables the liver cytochrome P450 system, the metabolism and biological response of the anti-carcinogenic flavonoid, quercetin, was examined. Profiling circulating metabolites revealed similar profiles over 72 h in wild type (WT) and POR-null (KO) mice, showing that hepatic P450 and reduced biliary secretion do not affect quercetin metabolism. Transcriptional profiling at 24 h revealed that 2-3 fold more genes responded significantly to quercetin in WT compared to KO in the jejunum, ileum, colon, and liver, suggesting that hepatic P450s mediate many of the biological effects of quercetin, such as immune function, estrogen receptor signaling and lipid, glutathione, purine, and amino acid metabolism, even though quercetin metabolism is not modified. The functional interpretation of expression data in response to quercetin (single dose of 7 mg/animal) revealed a molecular relationship between the liver and jejunum. In WT animals, amino acid and sterol metabolism were predominantly modulated in the liver, fatty acid metabolism response was shared between the liver and jejunum, and glutathione metabolism was modulated in the small intestine. In contrast, KO animals do not regulate amino acid metabolism in the liver or small intestine, they share the control of fatty acid metabolism between the liver and jejunum, and regulation of sterol metabolism is shifted from the liver to the jejunum and that of glutathione metabolism from the jejunum to the liver. This demonstrates that the quercetin-mediated regulation of these biological functions in extrahepatic tissues is dependent on the functionality of the liver POR. In conclusion, using a systems biology approach to explore the contribution of hepatic phase I detoxification on quercetin metabolism demonstrated the resiliency and adaptive capacity of a biological organism in dealing with a bioactive nutrient when faced with a tissue-specific molecular dysfunction. Keywords: nutritional intervention, comparative genomic response, genotype variation
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Project description:The role of innate immunity in modulating severity of chemotherapy-induced complications is so far unclear. The aim of this study was to determine how TLR2 may influence MTX-induced mucositis in the small intestine in mice. We used microarrays to assess gene expression profiles in proximal jejunum of WT vs. TLR2 KO mice after systemic treatment with MTX.
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Project description:RNA sequencing of pancres tissue of WT and IL23 expression mice (KSR23)
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Project description:Bulk RNA-seq of Intestine Epithelia (Jejunum, Ileum, Cecum and Colon) from Satb2-deficient and WT mice
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Project description:Using mice deficient in hepatic cytochrome-P450 oxidoreductase (POR), which disables the liver cytochrome P450 system, the metabolism and biological response of the anti-carcinogenic flavonoid, quercetin, was examined. Profiling circulating metabolites revealed similar profiles over 72 h in wild type (WT) and POR-null (KO) mice, showing that hepatic P450 and reduced biliary secretion do not affect quercetin metabolism. Transcriptional profiling at 24 h revealed that 2-3 fold more genes responded significantly to quercetin in WT compared to KO in the jejunum, ileum, colon, and liver, suggesting that hepatic P450s mediate many of the biological effects of quercetin, such as immune function, estrogen receptor signaling and lipid, glutathione, purine, and amino acid metabolism, even though quercetin metabolism is not modified. The functional interpretation of expression data in response to quercetin (single dose of 7 mg/animal) revealed a molecular relationship between the liver and jejunum. In WT animals, amino acid and sterol metabolism were predominantly modulated in the liver, fatty acid metabolism response was shared between the liver and jejunum, and glutathione metabolism was modulated in the small intestine. In contrast, KO animals do not regulate amino acid metabolism in the liver or small intestine, they share the control of fatty acid metabolism between the liver and jejunum, and regulation of sterol metabolism is shifted from the liver to the jejunum and that of glutathione metabolism from the jejunum to the liver. This demonstrates that the quercetin-mediated regulation of these biological functions in extrahepatic tissues is dependent on the functionality of the liver POR. In conclusion, using a systems biology approach to explore the contribution of hepatic phase I detoxification on quercetin metabolism demonstrated the resiliency and adaptive capacity of a biological organism in dealing with a bioactive nutrient when faced with a tissue-specific molecular dysfunction. Keywords: nutritional intervention, comparative genomic response, genotype variation
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Project description:Using mice deficient in hepatic cytochrome-P450 oxidoreductase (POR), which disables the liver cytochrome P450 system, the metabolism and biological response of the anti-carcinogenic flavonoid, quercetin, was examined. Profiling circulating metabolites revealed similar profiles over 72 h in wild type (WT) and POR-null (KO) mice, showing that hepatic P450 and reduced biliary secretion do not affect quercetin metabolism. Transcriptional profiling at 24 h revealed that 2-3 fold more genes responded significantly to quercetin in WT compared to KO in the jejunum, ileum, colon, and liver, suggesting that hepatic P450s mediate many of the biological effects of quercetin, such as immune function, estrogen receptor signaling and lipid, glutathione, purine, and amino acid metabolism, even though quercetin metabolism is not modified. The functional interpretation of expression data in response to quercetin (single dose of 7 mg/animal) revealed a molecular relationship between the liver and jejunum. In WT animals, amino acid and sterol metabolism were predominantly modulated in the liver, fatty acid metabolism response was shared between the liver and jejunum, and glutathione metabolism was modulated in the small intestine. In contrast, KO animals do not regulate amino acid metabolism in the liver or small intestine, they share the control of fatty acid metabolism between the liver and jejunum, and regulation of sterol metabolism is shifted from the liver to the jejunum and that of glutathione metabolism from the jejunum to the liver. This demonstrates that the quercetin-mediated regulation of these biological functions in extrahepatic tissues is dependent on the functionality of the liver POR. In conclusion, using a systems biology approach to explore the contribution of hepatic phase I detoxification on quercetin metabolism demonstrated the resiliency and adaptive capacity of a biological organism in dealing with a bioactive nutrient when faced with a tissue-specific molecular dysfunction. Keywords: nutritional intervention, comparative genomic response, genotype variation
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