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Genome-wide analysis of gene expression changes in mouse subcutaneous adipose tissue in cold compared to thermal neutrality

ABSTRACT: Comparison of gene expression pattern of subcutaneous adipose tissue from mice housed in cold (6-degree Celsius) or in thermal neutrality (30-degree celsius).Verify canonical white adipose tissue beiging pathways and genes that are regulated by cold-exposure as well as identify gap junction genes that are regulated by cold in white adipoes tissue.

ORGANISM(S): Mus musculus

PROVIDER: GSE84860 | GEO | 2016/07/27

SECONDARY ACCESSION(S): PRJNA335381

REPOSITORIES: GEO

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Genome-wide analysis of gene expression changes in mouse subcutaneous adipose tissue in cold compared to thermal neutrality

Project description:Comparison of gene expression pattern of subcutaneous adipose tissue from mice housed in cold (6-degree Celsius) or in thermal neutrality (30-degree celsius).Verify canonical white adipose tissue beiging pathways and genes that are regulated by cold-exposure as well as identify gap junction genes that are regulated by cold in white adipoes tissue. Total RNA obtained from mouse subcutaneous tissue from mice house at two different temperature; RNA extracted from 3-4 mice was pooled into one sample.

2016-07-27 | E-GEOD-84860 | biostudies-arrayexpress

Hyaluronan mediates cold-induced adipose tissue beiging

Project description:Adipose tissue beiging refers to a process through which beige adipocytes emerge in classical white adipose tissue depots. Beige adipocytes dissipate chemical energy and secrete adipokines like classical brown adipocytes to improve systemic metabolism, which offers benefits for people with obesity and metabolic diseases. Cold exposure and β3-adrenergic receptor (AR) agonist treatment are two commonly used stimuli for increasing beige adipocytes in mice, but their underlying biological processes are different. Transcriptional analysis of inguinal white adipose tissue (iWAT) has revealed that changes in extracellular matrix (ECM) pathway genes are specific to cold exposure. Hyaluronic acid (HA), a non-sulfated linear polysaccharide produced by nearly all cells, is one of the most common components of ECM. We found that cold exposure significantly increases iWAT HA levels while β3-AR agonist CL316,243 fails to do so. Increasing HA level in iWAT by Has2 overexpression significantly increases cold-induced adipose tissue beiging; in contrast, decreasing HA by Spam1 overexpression, which encodes a hyaluronidase that digests HA, significantly decreases cold-induced iWAT beiging. All of these data implicate a role of HA in promoting adipose tissue beiging that is unique to cold exposure. Given the failure of β3-AR agonists in clinical trials for obesity and metabolic diseases, increasing HA could serve as a new approach to recruiting more beige adipocytes to combat metabolic diseases.

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The cold exposure produce a different gene expression pattern in inguinal and periaortic white adipose

Project description:Male ferrets, aged 3 months, were divided into two group: one group remained at 22 degrees Celsius, while the other group was acclimatized to 4 degrees Celsius for one week. After sacrification, inguinal and periaortic white adipose tissues were dissected, and used for RNA isolation and subsequent global gene expression profiling using custom Agilent ferret-specific 2x400K microarrays. Data analysis indicated that while the cold exposure induces an increase on metabolism in inguinal white adopose tissue, in periaortic white adipose tissue this stimulus induces a reduction on expression of genes involved in cell cycle and in immune response.

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RNA-seq of cold stimulated inguinal fat of wild type and Rarres2-/- mice

Project description:Although various stimuli and mediators have been identified to promote thermogenic beige fat development, less is known about the negative regulator of cold-induced beiging. We here show that lack of chemerin that is highly expressed in white adipose tissue or its receptor CMKLR1 in adipocytes enhances cold-induced beiging and thermogenesis. Our results reveal a previously unrecognized beige-inhibitory role of chemerin-CMKLR1 axis, and suggests CMKLR1 as a therapeutic target for obesity-related metabolic disorders.

2019-12-31 | GSE133978 | GEO

Peripheral blood mononuclear cells as a source of cold exposure biomarkers

Project description:Male ferrets, aged 3 months, were divided into two group: one group remained at 22 degrees Celsius, while the other group was acclimatized to 4 degrees Celsius for one week. After sacrification, inguinal and periaortic white adipose tissues were dissected, and peripheral blood mononuclear cells (PBMC) were isolated. The three tissues are used for RNA isolation and subsequent global gene expression profiling using custom Agilent ferret-specific 2x400K microarrays. Data analysis indicated that the cold exposure induce a clear gene expression response of some genes in the inguinal and periaortic white adipose tissue as in PBMC. These genes could be defined as a biomakers of the effect of cold exposure in these cells.

2020-01-08 | GSE62352 | GEO

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Project description:The energy-burning capability of beige adipose tissue is a potential therapeutic tool for reducing obesity and metabolic disease, but this capacity is decreased by aging. Here, we evaluate the impact of aging on the profile and activity of adipocytes during the beiging process through single nucleus gene expression analysis of inguinal white adipose tissue of young and aged mice in response to cold exposure.

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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.

2021-04-07 | MSV000087164 | MassIVE

Genome-wide maps of gene expression in mouse Inguinal white adipose tissue

Project description:Using high throughput sequencing we report gene expression changes in mouse inguinal adipocytes from WT and Tet1 adipose-selective KO mice housed room temperature and exposed to 4 degree of cold for 4 hours

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METTL3-mediated Klf9 mRNA stabilization contributes to white adipose tissue beiging

Project description:The induction of beige adipocytes in white adipose tissue (WAT), also known as WAT beiging, improves glucose and lipid metabolism. However, the regulation of WAT beiging at the posttranscriptional level remains elusive. Here, we report that METTL3, the methyltransferase of N6-methyladenosine (m6A) mRNA modification, is induced during WAT beiging in mice. Adipose-specific depletion of Mettl3 gene undermines WAT beiging. Transcriptomic analysis of m6A modifications and mRNA expression level reveals global reduction of m6A-modified mRNAs in Mettl3-depleted beige adipose tissue. In particular, METTL3-catalyzed m6A installation on Krüppel-like factor 9 (Klf9) mRNA prevents its degradation. We further demonstrate that the m6A reader protein IGF2BP3 mediates the stabilization of m6A-modified Klf9 mRNA. Overexpressioin of KLF9 protein reverses the impaired WAT beiging elicited by Mettl3 deletion. These findings uncover a novel epitranscriptional mechanism in WAT beiging and identify METTL3-KLF9 axis as a potential therapeutic target for obesity-associated disorders.

2023-02-03 | GSE178884 | GEO

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