White adipose tissue resident macrophages are required for adipogenesis and energy storage.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA415569 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6207050.fastq.gz | Fastqsanger.gz | |||
| SRR6207060.fastq.gz | Fastqsanger.gz | |||
| SRR6207070.fastq.gz | Fastqsanger.gz | |||
| SRR6207051.fastq.gz | Fastqsanger.gz | |||
| SRR6207061.fastq.gz | Fastqsanger.gz |
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Project description:White adipose tissue (WAT) stores energy in the form of lipids. WAT macrophages cause adipose tissue inflammation and insulin resistance when intake exceeds expenditures, but their contribution to homeostasis remain poorly understood. Here, we show that two populations, ã and ä, of TNF-producing bone marrow-derived monocytic cells are transiently recruited to damaged adipocytes and mediate insulin resistance. In contrast, we identify α/β yolk-sac derived resident macrophages that produce adipogenic growth factors, and form a niche required for adipogenesis as white adipocytes do not differentiate in their absence. Production of adipogenic growth factors by α/β macrophages increases with lipid storage, but they do not contribute to inflammation. Thus the molecular identities and functions of resident macrophages and BM-derived cells are specified by their lineage rather than diet variation. These results identify an essential function of WAT resident macrophages in adipogenesis and energy homeostasis, separate from inflammation mediated by the recruitment of inflammatory leukocytes.
2020-10-24 | GSE106084 | GEO
Project description:Purpose: The goals of this experiment were to examine the transcriptional profiles (RNA-seq) of inguinal white adipose tissue (iWAT) in mice subjected to the indicated diets and treatments for eight weeks. Methods: 6-week-old C57BL6/J mice fed a control or a high-fat diet were treated with anti-PDGFcc neutralizing antibodies or Goat IgG for 2 weeks of treatment. Antibodies were administered by i.p. every two days. Four animals were treated in each condition. The resulting iWAT from these mice were sequenced in duplicates, aligned with STAR, quantified with featureCounts, and then differential gene expression analyses were performed using limma. Results: An unbiased analysis of hallmark pathways in iWAT of anti-PDGFcc antibody-treated mice and control animals using a pre-ranked Gene Set Enrichment Analysis (GSEA) identified adipogenesis as the pathway most differentially regulated by PDGFcc blockade when accounting for diet effects. By contrast, the hallmark fatty acid metabolism pathway which includes genes involved in lipid uptake, lipid oxidation, and lipid mobilization was not significantly enriched after anti-PDGFcc treatment. Similarly, hallmark pathways glycolysis, MTORC1 signaling, or TGFb signaling were not differentially regulated by anti-PDGFcc treatment after accounting for diet effects. An additional GSEA analysis of genes involved in lipid synthesis and storage identified a subset of genes up-regulated by PDGFcc blockade regardless of diet, which included several negative regulators of lipid synthesis and storage such as Insig1, Ppara, and Idh2. Conclusions: A GSEA identified adipogenesis as the pathway most differentially regulated by PDGFcc blockade when accounting for diet effects. Key genes involved included several negative regulators of lipid synthesis and storage such as Insig1, Ppara, and Idh2.
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Project description:Since the worldwide increase in obesity represents a growing challenge for the health care systems, new approaches are needed to treat obesity and associated disease effectively. The food intake is primarily stored in the adipose tissue and therefore this organ is in focus to develop new anti-obesity treatments. To provide a systematic analysis of genes that regulate adipose tissue biology and to establish a target-oriented compound screening, we performed a high throughput siRNA screen with primary (pre)adipocytes, using a druggable siRNA library targeting 7,784 human genes. Beside well known regulators of adipogenesis and neutral lipid storage (like PPAR?, RXR, Perilipin A) the screening revealed a large number of genes which were not previously described in the context of fatty tissue biology. An enrichment of genes was observed for axonemal dyneins. Five out of ten anxonemal dyneins were identified in our primary screen and retested positive with independent siRNAs and cell-donors. Quantitative RT-PCR- and immunoblot analysis revealed that axonemal dyneins are expressed in preadipocytes and maturing adipocytes. Using microarray analysis, we further characterize the remaining genes identified in our primary screen to determine their expression pattern during adipogenesis. In the course of fat cell differentiation, 149 among the 459 positive genes were regulated on the gene expression level. Assuming that an adipogenesis-specific expression pattern is another independent hind, that these genes are involved in neutral lipid storage and/or adipocyte differentiation, we retested this gene-pool with independent siRNAs and cell donors. Finally, to show that the genes identified are per se druggable we performed a proof of principle experiment using an antagonist for one randomly chosen gene. The results showed a very similar phenotype compared to knock-down experiments proofing the druggability. Thus, we identified new adipogenesis-associated genes and those involved in neutral lipid storage. Moreover, by using a druggable siRNA library the screen data provides a very attractive starting point, to identify anti-obesity compounds targeting the adipose tissue. For microarray analysis, RNA was isolated at 3 different points in time during adipogenesis (day 0, day 3 and day 7 after induction of differentiation). This experiment was carried out with cells obtained from three different donors. No replicates are included for each point in time.
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Project description:Since the worldwide increase in obesity represents a growing challenge for the health care systems, new approaches are needed to treat obesity and associated disease effectively. The food intake is primarily stored in the adipose tissue and therefore this organ is in focus to develop new anti-obesity treatments. To provide a systematic analysis of genes that regulate adipose tissue biology and to establish a target-oriented compound screening, we performed a high throughput siRNA screen with primary (pre)adipocytes, using a druggable siRNA library targeting 7,784 human genes. Beside well known regulators of adipogenesis and neutral lipid storage (like PPAR?, RXR, Perilipin A) the screening revealed a large number of genes which were not previously described in the context of fatty tissue biology. An enrichment of genes was observed for axonemal dyneins. Five out of ten anxonemal dyneins were identified in our primary screen and retested positive with independent siRNAs and cell-donors. Quantitative RT-PCR- and immunoblot analysis revealed that axonemal dyneins are expressed in preadipocytes and maturing adipocytes. Using microarray analysis, we further characterize the remaining genes identified in our primary screen to determine their expression pattern during adipogenesis. In the course of fat cell differentiation, 149 among the 459 positive genes were regulated on the gene expression level. Assuming that an adipogenesis-specific expression pattern is another independent hind, that these genes are involved in neutral lipid storage and/or adipocyte differentiation, we retested this gene-pool with independent siRNAs and cell donors. Finally, to show that the genes identified are per se druggable we performed a proof of principle experiment using an antagonist for one randomly chosen gene. The results showed a very similar phenotype compared to knock-down experiments proofing the druggability. Thus, we identified new adipogenesis-associated genes and those involved in neutral lipid storage. Moreover, by using a druggable siRNA library the screen data provides a very attractive starting point, to identify anti-obesity compounds targeting the adipose tissue.
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Project description:lncRAP2 is a conserved cytoplasmic lncRNA enriched in adipose tissue and required for adipogenesis. Using purification and in vivo interactome analyses, we show that lncRAP2 forms complexes with proteins that stabilize mRNAs and modulate translation, among them Igf2bp2. Surveying transcriptome-wide Igf2bp2 client mRNAs in white adipocytes reveals selective binding to mRNAs encoding adipogenic regulators and energy expenditure effectors, including Adiponectin. These same target proteins are downregulated when either Igf2bp2 or lncRAP2 is downregulated, hindering adipocyte lipolysis. Proteomics and ribosome profiling show this occurs predominantly through mRNA accumulation, as lncRAP2-Igf2bp2 complex binding does not impact translation efficiency. Phenome-wide association studies reveal specific associations of genetic variants within both lncRAP2 and Igf2bp2 with body mass and type 2 diabetes, and both lncRAP2 and Igf2bp2 are suppressed in adipose depots of obese and diabetic individuals. Thus, the lncRAP2-Igf2bp2 complex potentiates adipose development and energy expenditure and is associated with susceptibility to obesity-linked diabetes.
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Project description:lncRAP2 is a conserved cytoplasmic lncRNA enriched in adipose tissue and required for adipogenesis. Using purification and in vivo interactome analyses, we show that lncRAP2 forms complexes with proteins that stabilize mRNAs and modulate translation, among them Igf2bp2. Surveying transcriptome-wide Igf2bp2 client mRNAs in white adipocytes reveals selective binding to mRNAs encoding adipogenic regulators and energy expenditure effectors, including Adiponectin. These same target proteins are downregulated when either Igf2bp2 or lncRAP2 is downregulated, hindering adipocyte lipolysis. Proteomics and ribosome profiling show this occurs predominantly through mRNA accumulation, as lncRAP2-Igf2bp2 complex binding does not impact translation efficiency. Phenome-wide association studies reveal specific associations of genetic variants within both lncRAP2 and Igf2bp2 with body mass and type 2 diabetes, and both lncRAP2 and Igf2bp2 are suppressed in adipose depots of obese and diabetic individuals. Thus, the lncRAP2-Igf2bp2 complex potentiates adipose development and energy expenditure and is associated with susceptibility to obesity-linked diabetes.
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