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RNA-seq of gonadal adipose tissue from male and female Trim28-WT and Trim28 adipose specific KO mice

ABSTRACT: RNA-seq of gonadal adipose tissue from male and female Trim28-WT and Trim28 adipose specific KO mice

PROVIDER: PRJEB41526 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4873300.fastq.gz	Fastqsanger.gz
	ERR4873310.fastq.gz	Fastqsanger.gz
	ERR4873320.fastq.gz	Fastqsanger.gz
	ERR4873301.fastq.gz	Fastqsanger.gz
	ERR4873311.fastq.gz	Fastqsanger.gz

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RNA-seq of gonadal adipose tissue from male and female Trim28-WT and Trim28 adipose specific KO mice

Project description:Many genes have been implicated in WAT lipid metabolism, including tripartite motif containing 28 (Trim28), a gene proposed to primarily influence adiposity via epigenetic mechanisms in embryonic development. We set out to determine if adipose specific deletion of Trim28 led to changes in adipose tissue function and molecular phenotype. We performed transcriptomics analysis on adipose tissue taken from WT and adipose specific Trim28 KO mice to investigate their molecular phenotype, and to identify pathways altered in KO animals.

2020-11-25 | E-MTAB-9809 | biostudies-arrayexpress

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Project description:We identified secreted frizzled-related protein-5 (Sfrp5) as a transcript that is upregulated during adipocyte differentiation and that is increased in white adipose tissue (WAT) of obese mice, compared to lean mice. To investigate the function of sFRP5 in adipose tissue biology, we studied sFRP5Q27stop mice, in which ENU mutagenesis was used to create a premature stop codon at Gln27, thereby creating a likely null allele. Male wild-type or Sfrp5 KO (Q27Stop) mice were fed a high-fat diet from the ages of four weeks to twelve weeks. At twelve weeks of age, mice were euthanized. Total RNA was then isolated from gonadal WAT and RNA was analyzed by Affymetrix microarrays. Seven wild-type and eight Sfrp5 KO mice were used.

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Project description:A microarray study was performed in unstimulated and TCR-stimulated CD4 + T cells and Treg in wild type and conditional Trim28 KO mice to identify genes that are regulated by Trim28. These experiments constitute a portion of the study described below: Paper Abstract: Peripheral T cell activation and differentiation into specialized effectors are regulated by TCR- and cytokine-mediated signals that induce clonal expansion and unique transcriptional factors. These processes may include active chromatin modification by nuclear factors. In search of such molecules, we found Trim28, a component of large nuclear chromatin-regulatory complex is tightly controlled upon TCR stimulation at the level of phosphorylation, and examined global impact of Trim28 loss in especially CD4+ T cells, by generating T cell-specific conditional Trim28 KO mice (CKO). CD4+ T cells from CKO mice showed defective IL-2 production and T cell proliferation associated with defective upregulation of cell-cycle associated proteins. Accordingly, young CKO showed T-lymphopenia. Surprisingly, Trim28 CKO mice eventually accumulated auto-reactive memory-phenotype T cells that produced inflammatory IL-17. CKO mice are also susceptible to induced auto-inflammatory disease with TH-17 dominant immune response. Loss of Trim28 showed aberrant accumulation of TH-17 and FoxP3+ T cells, two key T cells in inflammation vs. tolerance. We found CKO T cells showed a cell-extrinsic promotion of TH-17 and FoxP3+ T cell development by a mechanism involving overproduction of TGF-beta. Our study revealed unexpected roles of Trim28, a global chromatin regulator in both T cell activation and tolerance. Trim28 conditional KO mice and age-matched control mice were sacrificed, and neive CD4+ T cells (CD4+CD62+CD25-) and Treg (CD4+CD62+CD25+) were sorted. Stimulation of naive T cells was done with anti-CD3 and anti-CD28 for 13 hours. We collected quadruplicates for each group.

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