Mus musculus strain:C57BL/6j
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA470640 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7154852.fastq.gz | Fastqsanger.gz | |||
| SRR7154853.fastq.gz | Fastqsanger.gz | |||
| SRR7154854.fastq.gz | Fastqsanger.gz | |||
| SRR7154855.fastq.gz | Fastqsanger.gz | |||
| SRR7154856.fastq.gz | Fastqsanger.gz |
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Project description:Endothelial cells (ECs) have been reported to be a source of adipose tissue-derived stromal cells (ADSCs), and ADSCs expressing endothelial markers have been suggested to originate from ECs. To further investigate the lineage relationship between ECs and ADSCs in postnatal mice, we performed single-cell RNA sequencing (scRNA-seq) on ECs and ADSCs isolated from inguinal and gonadal white adipose tissues (IWATs and GWATs) of 12-week-old wild-type C57BL/6J mice, and analyzed the expression of endothelial markers in ADSCs.
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Project description:RNA-seq analysis of inguinal white adipose tissue from mice administered 3 PPA under cold conditions for 14 days
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Project description:Adipose tissue depots vary markedly in their ability to store and metabolize triglycerides, undergo beige adipogenesis and be susceptibile to metabolic disease. The molecular mechanisms that underlie such heterogeneity are not entirely clear. Previously, we showed that TGF-b signaling regulates the browning of white adipose tissue via recruitment of dedicated beige progenitors. Here, we find that TGF-b signals dynamically regulate the balance between adipose tissue fibrosis and beige adipogenesis. Elevated basal and high-fat diet inducible activation of TGF-b/Smad3 signaling was observed in the visceral (epididymal) adipose tissue depot. Activation of TGF-b/Smad3 signaling was associated with increased adipose tissue fibrosis. RNA-seq combined with fluorescence-activated cell sorting of stromal vascular fraction of epididymal white adipose tissue depot resulted in identification of TGF-b/Smad3 regulated ITGA5+ fibrogenic progenitors. TGF-b/Smad3 signal inhibition, genetically or pharmacologically, reduced fibrosis and increased functional beige adipogenesis. TGF-b/Smad3 antagonized the beneficial effects of PPARγ , activation whereas TGF-b receptor 1 inhibition synergized with actions of rosiglitazone, a PPARγ agonist, to dampen fibrosis and promote beige adipogenesis. There was a positive correlation between TGF-b activation and levels of fibrosis marker, ITGA5, in human adipose tissue samples , with visceral (omental) adipose tissue depot exhibiting higher fibrosis potential than subcutaneous or brown adipose tissue depots. Taken together, out data provide TGF-b/Smad3 signaling operates at the nexus of adipose tissue fibrosis and functional beige adipogenesis.
2025-09-01 | GSE268791 | GEO
Project description:To systemically determine the translational control of gene expression in adipose, we performed ribosome profiling and RNA-seq in parallel to depict the translatome and transcriptome changes during primary brown and white adipogenesis, and between brown and white adipose tissue.
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Project description:Here we provide scRNAseq data from the stromal vascular fraction of adult (8 weeks) murine brown adipose tissue. This allows studying cellular composition and cellular heterogeneity within brown fat.
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Project description:Abstract
Brown and brite adipocytes are the key cells performing uncoupling protein 1 (UCP1) dependent non-shivering thermogenesis (NST) induced by cold exposure. Several lipid species are associated to NST in brown and white adipose tissue. Studies investigating the association of the lipid profile with NST rely on the analysis of whole organ homogenates or on the differentiation of pre-adipocytes in vitro. These approaches have so far not addressed the heterogeneity of white adipose tissue. Aim of this study was to characterize the lipid composition of white adipose tissue on a region-specific level in an in vivo context.
We applied MALDI mass spectrometry imaging (MALDI-MSI) in combination with immunohistochemistry and high-resolution mass spectrometry on sections of inguinal white adipose tissue of 129S6/SvEvTac and C57BL6/N-UCP1 knockout and wildtype mice acclimatized to cold to identify lipids specific to areas of UCP1 expression.
Based on the analysis of cold exposed 129S6/SvEvTac mice we identified cardiolipins (CL) and diacylglycerols (DG) species to be specific for areas expressing UCP1 and triacylglycerols (TG) to be the main lipid class characteristic for UCP1 negative regions within inguinal white adipose tissue. Investigation of C57BL6/N-UCP1 knockout and wildtype mice housed at either room temperature or acclimatized to cold, demonstrated that CL content in white adipose tissue is increased upon cold stimulation, independent of UCP1.
We introduce a MALDI-MSI based approach to identify lipids associated to thermogenic adipocytes in adipose tissues demonstrating a clear regional cold dependent upregulation of CL independent of UCP1.
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Project description:We used microarrays to detail the gene expression profile during WAT -beige transition by treatment of beta adrenergic receptor agonist . Stromal vascular fractions (SVF) from mice (n = 3/group) that received vehicle or beta3 adrenergic receptor agonist, CL, treatment were served for RNA extraction and hybridization on Affymetrix microarrays. We are trying to find out angiogenic factors genes dynamics during white adipose tissues (WAT) - beige transition.
2014-03-15 | E-GEOD-55934 | biostudies-arrayexpress
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2019-09-09 | GSE124279 | GEO
Project description:Human antigen R (HuR) protein, a RNA binding protein (RBP), has been reported to regulate essential steps in RNA metabolism and immune response in a variety of cell types, but its function in metabolism remains unclear. This study identifies HuR as a major repressor during adipogenesis. Knockdown and overexpression of HuR in primary adipocyte culture enhances and inhibits adipogenesis in vitro, respectively. Fat-specific knockout of HuR significantly enhances adipogenic gene program in all three major adipose tissues including epidydimal, inguinal white and brown adipose tissue, accompanied with systemic glucose intolerance and insulin resistance. Conversely, transgenic overexpression of HuR in adipose tissue prevents the HFD induced obesity by repressing adipogenesis. Mechanistically, HuR may inhibit adipogenesis by recognizing and modulating the stability of hundreds of adipocyte transcripts, including the mRNA of Insig1, a negative regulator during adipogenesis. Taken together, our work establishes HuR as a novel posttranscriptional regulator of adipogenesis and provides a new insight into how RNA processing contributes to adipocyte development.
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