Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity
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ABSTRACT:
PROVIDER: PRJNA134139 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE25401: Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [gene expression] GSE25470: Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [miRNA data] GSE25910: Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [differentiation data] Refer to individual Series
2012-08-12 | E-GEOD-25402 | biostudies-arrayexpress
Project description:We used an unbiased systems biology approach to study the regulation of gene expression in human adipose tissue focusing on inflammation. We show that microRNAs play a major role as regulators of CCL2 production in obesity.
2012-08-13 | GSE25910 | GEO
Project description:We used an unbiased systems biology approach to study the regulation of gene expression in human adipose tissue focusing on inflammation. We show that microRNAs play a major role as regulators of CCL2 production in obesity.
2012-08-13 | GSE25470 | GEO
Project description:We used an unbiased systems biology approach to study the regulation of gene expression in human adipose tissue focusing on inflammation. We show that microRNAs play a major role as regulators of CCL2 production in obesity.
2012-08-13 | GSE25401 | GEO
Project description:We used an unbiased systems biology approach to study the regulation of gene expression in human adipose tissue focusing on inflammation. We show that microRNAs play a major role as regulators of CCL2 production in obesity. Abdominal subcutaneous adipose needle biopsies were obtained from women (n=56) with a wide variation in BMI. From the biopsies we prepared and hybridised biotinylated complementary RNA to GeneChip Human Gene 1.0 ST Arrays (Affymetrix Inc., Santa Clara, CA), labelled RNA to Affymetrix miRNA arrays, and bisulphite converted DNA to Illumina Infinium HumanMethylation27 beadchips using standardised protocols (Affymetrix Inc., Illumina Inc.) . Subsequent analyses of gene expression was performed using the Affymetrix GeneChip Operating Software version 1.4. To allow comparisons of transcript levels between samples, all samples were subjected to an all-probeset scaling-to-target signal of 100.
2012-08-12 | E-GEOD-25401 | biostudies-arrayexpress
Project description:We used an unbiased systems biology approach to study the regulation of gene expression in human adipose tissue focusing on inflammation. We show that microRNAs play a major role as regulators of CCL2 production in obesity. Abdominal subcutaneous adipose needle biopsies were obtained from women (n=56) with a wide variation in BMI. From the biopsies, total RNA was isolated and labelled using the FlashTag biotin HSR labeling kit (Genisphere Inc., Hatfield, PA) according to the supplier's protocol. The labelled samples were placed in a hybridization cocktail mix containing 4% formamide and hybridised overnight to Affymetrix miRNA Arrays (Affymetrix Inc.) following the indicated Genisphere protocol. The arrays were washed, stained and scanned in an Affymetrix GCS 3000 scanner. Signal intensities and present calls were generated by using the microRNA QC tool by Affymetrix.
2012-08-12 | E-GEOD-25470 | biostudies-arrayexpress
Project description:We used an unbiased systems biology approach to study the regulation of gene expression in human adipose tissue focusing on inflammation. We show that microRNAs play a major role as regulators of CCL2 production in obesity. Subcutaneous adipose tissue was obtained from healthy subjects undergoing cosmetic liposuction (n=12). There was no selection for age, sex or BMI. From the tissue, we isolated preadipocytes and in vitro differentiated them to adipocytes. The cells were lysed at day 4/5 (early), 8 (middle) and 12 (late) of differentiation. From the samples, we prepared and hybridised biotinylated complementary RNA to GeneChip Human Gene 1.0 ST Arrays (Affymetrix Inc., Santa Clara, CA). Pre-processing was performed using the Affymetrix Expression Console version 1.1 and the following settings: Summarization: PLIER; Background Correction: PM-GCBG; Normalization: Global Median.
2012-08-12 | E-GEOD-25910 | biostudies-arrayexpress
Project description:In obesity, white adipose tissue (WAT) inflammation is linked to insulin resistance. Increased adipocyte chemokine (C-C motif) ligand 2 (CCL2) secretion may initiate adipose inflammation by attracting the migration of inflammatory cells into the tissue. Using an unbiased approach, we identified adipose microRNAs (miRNAs) that are dysregulated in human obesity and assessed their possible role in controlling CCL2 production. In subcutaneous WAT obtained from 56 subjects, 11 miRNAs were present in all subjects and downregulated in obesity. Of these, 10 affected adipocyte CCL2 secretion in vitro and for 2 miRNAs (miR-126 and miR-193b), regulatory circuits were defined. While miR-126 bound directly to the 3'-untranslated region of CCL2 mRNA, miR-193b regulated CCL2 production indirectly through a network of transcription factors, many of which have been identified in other inflammatory conditions. In addition, overexpression of miR-193b and miR-126 in a human monocyte/macrophage cell line attenuated CCL2 production. The levels of the two miRNAs in subcutaneous WAT were significantly associated with CCL2 secretion (miR-193b) and expression of integrin, α-X, an inflammatory macrophage marker (miR-193b and miR-126). Taken together, our data suggest that miRNAs may be important regulators of adipose inflammation through their effects on CCL2 release from human adipocytes and macrophages.
| S-EPMC3402332 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2012-08-13 | GSE25402 | GEO
Project description:Obesity is associated with chronic low-grade white adipose tissue (WAT) inflammation that can contribute to the development of insulin resistance in mammals. Previous studies have identified interleukin (IL)-12 as a critical upstream regulator of WAT inflammation and metabolic dysfunction during obesity, however, the cell types and mechanisms that initiate WAT IL-12 production remain unclear. Analysis of mouse and human WAT single cell transcriptomic datasets, IL-12 reporter mice, and IL-12p70 protein levels by ELISA identified activated conventional type 1 dendritic cells (cDC1s) as the cellular source of WAT IL-12 during diet-induced obesity. cDC1s were required for the development of obesity-associated inflammation by increasing group 1 innate lymphocyte interferon (IFN)-γ production and inflammatory macrophage accumulation. Inducible depletion of cDC1s increased WAT insulin sensitivity and systemic glucose tolerance during diet-induced obesity. Endocytosis of apoptotic bodies containing self-DNA by WAT cDC1 drove STING-dependent IL-12 production. Together, these results suggest that WAT cDC1s act as critical regulators of adipose tissue inflammation and metabolic homeostasis during obesity.
2024-06-30 | GSE236110 | GEO