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Mus musculus

ABSTRACT: Egr1 deficiency induces browning of inguinal subcutaneous white adipose tissue in mice

PROVIDER: PRJNA356754 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5088690.fastq.gz	Fastqsanger.gz
	SRR5088691.fastq.gz	Fastqsanger.gz
	SRR5088692.fastq.gz	Fastqsanger.gz
	SRR5088693.fastq.gz	Fastqsanger.gz
	SRR5088694.fastq.gz	Fastqsanger.gz

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Expression data from browning inguinal white adipose tissue in UCP1/ApoE-DKO mice

Project description:Differentiation of brown adipocytes is a crucial process for adaptive thermogenesis, which is stimulated by various factors. We found robust browning of inguinal white adipose tissue in UCP1/ApoE-DKO mice, but not in ApoE-KO mice, under high-fat diet condition. We used microarray to determine the genes specifically regulated in the browning white adipose tissue in UCP1/ApoE-DKO mice.

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Interaction between PPARγ and mTORC1 in the regulation of inguinal white adipose tissue transcriptome

Project description:Purpose: To investigate the involvement of mTORC1 as a mediator of the actions of the PPARγ ligand rosiglitazone in subcutaneous inguinal white adipose tissue transcriptome; Methods: Mice bearing regulatory associated protein of mTOR (Raptor) deletion and therefore mTORC1 deficiency exclusively in adipocytes (adiponectin Cre recombinase) and littermate controls were fed a high-fat diet supplemented or not with the PPARγ agonist rosiglitazone (30 mg/kg/day) for 8 weeks and evaluated for inguinal white adipose tissue transcriptome (Rnaseq); Results: 3,2425 genes had their correspondent mRNA levels altered by either adipocyte Raptor deficiency or rosiglitazone administration or their combination. Among those, 408 genes modulated by rosiglitazone required mTORC1. Conclusion: PPARγ and mTORC1 are essential partners in the regulation of a cluster of genes in inguinal white adipose tissue.

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Project description:Visceral white adipose tissue is closed correlated with obesity and metabolic dysfunction. Epididymal adipose tissue (eWAT) is considered as typical visceral white adipose tissue. Induction of browning of white adipose tissue improves metabolic dysfunction such as insulin resistance. In contrast to mice subcutaneous adipose tissue, visceral fat do not show significant browning under 4°C. However,under physiologically tolerable low temperature visceral adipose tissue can turn brown. We used microarrays to detail the global programme of gene expression in C57Bl/6 mice epididymal adipose tissue exposed to thermoneutral 30°C, 4°C and temperatures lower than 4°C.

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Project description:Selective ablation of Hdac3 in adipose tissue switches the metabolic signature of white adipose tissue by potentiating oxidative capacity and boosting browning. To investigate the genome-wide consequences of the lack of Hdac3 in adipose tissue, we used RNA-seq to profile the gene expression program of inguinal adipose tissue from mice with selective ablation of Hdac3 in adipose tissue (H3atKO) and their respective control (floxed).

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Project description:We investigated gene expression signatures in subcutaneous inguinal adipose tissue obtained from wild type and R6/2 mice with the aim to identify gene expression changes and signalling pathway alterations in adipose tissue relevant to HD. Gene expression was assessed using Affymetrix GeneChipÂ® Mouse Gene 2.0 ST Array. Target genes were technically validated using real-time quantitative PCR. 12 subcutaneous inguinal white adipose tissue samples were analyzed by affymetrix: 6 wild-type samples; 6 R6/2 mouse samples.

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Project description:To determine the function of miR-203 in white fat browning upon cold exposure, we injected miR-203 inhibitors and negative control into inguinal white adipose tissue, followed by cold exposure (4oC) for 24 hours. Total RNA were harvested for RNA-seq.

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A non-cell autonomous mechanism of beige adipocyte renaissance in subcutaneous adipose tissue

Project description:Two types of UCP1 positive cells-brown and beige adipocytes exist in mammals. Beige adipocytes are very plastic, and can be dynamically regulated by environment.Beige adipocytes formed postnatally in subcutaneous inguinal white adipose tissue (iWAT) lost thermogenic gene expression and multilocular morphology at adult stage, but cold could restore their “beigeing” characteristics, a phenomenon termed as beige adipocyte renaissance. Our results showed that beige cell maintenance and renaissance in adult mice were regulated by cAMP and HDAC4 signaling in white adipocytes non-cell autonomously. Genetic modulations of various components of this cAMP-HDAC4 cascade (e.g. LKB1) led to persistent browning and reduced adiposity independent of thermogenesis. To further study the mechanisms of beige adipocytes maintenance, we performed RNA-seq with samples from inguinal white adipose tissues of WT, AdipoqCre LKB1 F/F, and AdipoqCre LKB1 F/F; HDAC4 F/F mice.Our studies will move the beige adipocyte field forward and attract clinical applications to target beige adipocyte renaissance.

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