Diet-induced obesity dysregulates rapid epigenetic response to hypoxia in macrophages (RNA-Seq)
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ABSTRACT:
PROVIDER: PRJNA970373 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24471349.fastq.gz | Fastqsanger.gz | |||
| SRR24471350.fastq.gz | Fastqsanger.gz | |||
| SRR24471351.fastq.gz | Fastqsanger.gz | |||
| SRR24471352.fastq.gz | Fastqsanger.gz | |||
| SRR24471353.fastq.gz | Fastqsanger.gz |
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Project description:Diet-induced obesity dysregulates rapid epigenetic response to hypoxia in macrophages (ChIP-Seq)
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Project description:Macrophages play important roles in tissue homeostasis and tissue healing process. The response to hypoxic environment is a trigger to induce key signaling pathways in macrophages. Functions of macrophages are dysregulated in metabolic diseases such as diabetes and obesity resulting in poor tissue healing. Epigenetic status including histone modification in macrophages is regulated by hypoxia. However, whether and how obesity influences histone modification under hypoxia is unknown. Using chromatin immunoprecipitation-sequencing (ChIP-seq), RNA-seq on mouse bone marrow-derived macrophages, we sought to determine whether hypoxia alters histone 3-lysine 4 trimethylation (H3K4me3) and gene expression profile in macrophages and how obesity influences H3K4me3 enrichment on the genome in hypoxia-dependent and -independent manner.
2024-05-05 | GSE231991 | GEO
Project description:Macrophages play important roles in tissue homeostasis and tissue healing process. The response to hypoxic environment is a trigger to induce key signaling pathways in macrophages. Functions of macrophages are dysregulated in metabolic diseases such as diabetes and obesity resulting in poor tissue healing. Epigenetic status including histone modification in macrophages is regulated by hypoxia. However, whether and how obesity influences histone modification under hypoxia is unknown. Using chromatin immunoprecipitation-sequencing (ChIP-seq), RNA-seq on mouse bone marrow-derived macrophages, we sought to determine whether hypoxia alters histone 3-lysine 4 trimethylation (H3K4me3) and gene expression profile in macrophages and how obesity influences H3K4me3 enrichment on the genome in hypoxia-dependent and -independent manner.
2025-05-05 | GSE231992 | GEO
Project description:Hypoxia is the most common adverse event during gastrointestinal endoscopes sedated with propofol and sufentanil, especially in obese people. In the present study, high-flow nasal cannula oxygenation will be utilized in order to reduce the incidence of hypoxia among obesity.
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Project description:Hypoxia dysregulates circadian rhythm and causes synapse elimination defects in astrocytes
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Project description:Recently white adipose tissues (WAT) have been shown to be able to generate heat upon cold exposure through the expression of uncoupling protein-1 (UCP1), a molecule regulating mitochondrial proton gradient. Although the role of UCP1 has been extensively investigated in adipocytes, it is currently unknown whether UCP1 in the microenvironment of WAT such as adipose-tissue macrophages (ATM) could play a role in thermogenesis. Given the critical role of hypoxia in regulating obesity and insulin resistance, we challenged our myeloid-specific hypoxia-inducible factor-1α (Hif-1α) knockout (KO) mice to high fat diet and observed that these mice were not only protected from diet-induced obesity but also resistant to the body temperature changes upon cold exposure, the latter effect being completely lost upon surgical removal of WAT. Mechanistically, ATM deficient for HIF-1α generated heat production through increased expression of UCP1 and increased mitochondrial functions, all of which lead to an enhanced lipolysis in neighboring adipocytes. Lastly, we observed a number of co-localized areas between UCP-1 and CD68 in WAT of lean mice as well as individuals whereas such areas were not observed in an obese mice or human subjects. In conclusion, we demonstrate a novel mechanism by which ATM regulate obesity through UCP1-mediated heat generation.
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Project description:Obesity exacerbates inflammation upon lung injury; however, the mechanisms by which obesity primes pulmonary dysregulation prior to injury are not well studied. Notably, little is known about how obesity dysregulates pulmonary polyunsaturated fatty acid (PUFA) metabolism that is central to inflammation initiation and resolution. Herein, we first show that a high fat diet (HFD) administered to C57BL/6J mice increases the relative abundance of pulmonary PUFA-containing triglycerides and the concentration of PUFA-derived oxylipins, independent of an increase in total pulmonary PUFAs, prior to onset of pulmonary inflammation. Experiments with a genetic model of obesity did not recapitulate the effects of the HFD on the pulmonary oxylipin signature, revealing a diet-driven effect. Subsequent pulmonary next-generation RNA sequencing identified complex and unique transcriptional regulation with the HFD. The HFD increased pathways related to glycerophospholipid metabolism and immunity, including an elevation in B cell differentiation and signaling. Finally, computational integration of lipidomic with transcriptomic data revealed novel HFD-driven networks between glycerophospholipid metabolism and B cell receptor signaling with specific PUFA-derived oxylipins. Collectively, these data show obesity dysregulates pulmonary PUFA metabolism prior to lung injury, which may be a mechanism by which obesity primes the lungs to respond poorly upon infectious and/or inflammatory challenges.
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Project description:Macrophages are primary immune cells involved in obesity-triggered chronic low-grade inflammation in adipose tissues. Prostaglandin (PG) E2, mainly generated from macrophages, can regulate adipose tissue remodeling. Here, we observed that PGE2 receptor subtype 3 (EP3) was remarkably downregulated in adipose tissue macrophages from high-fat diet (HFD)-fed mice and patients with obesity. Notably, macrophage-specific deletion of EP3 exacerbated HFD-induced obesity in mice, whereas EP3α isoform overexpression in macrophages alleviated obesity phenotype in HFD-fed mice. EP3 deficiency suppressed anti-adipogenic secreted protein acidic and rich in cysteine (SPARC) secretion in macrophages. SPARC deletion in macrophages abrogated the protection of EP3α-overexpression against HFD-induced obesity in mice. Mechanistically, EP3 activation promoted SPARC expression by suppressing DNA methylation in macrophages through the PKA/Sp1/Dnmt1/3a signaling cascade. EP3 agonist treatment ameliorates HFD-induced obesity in mice. Thus, EP3 inhibits adipogenesis through promoting macrophage releasing SPARC and may serve as a therapeutic target for managing diet-induced obesity.
2025-05-25 | PXD063443 | Pride
Project description:Obesity is associated with adverse airway events including desaturation during deep sedation. Previous studies have suggested that high-flow nasal oxygenation may be superior to regular (low-flow) nasal cannula for prevention of hypoxia during Sedated Gastrointestinal Endoscopy in non-obesity patients. The prerequisite of high-flow nasal oxygenation is keeping airway patency. Our pervious study demonstrated that nasopharyngeal airway has the similar efficacy of jaw-lift. In present study we aimed to determine whether high-flow nasal oxygenation combined with nasopharyngeal airway could reduce the incidence of hypoxia during Sedated Gastrointestinal Endoscopy in obese patients.
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Project description:Diet-induced obesity impairs mitochondrial respiratory responses in tissues that are highly metabolically active, such as the heart. However, less is known about the impact of obesity on the respiratory activity of specific cell types, such as splenic B cells. B cells are of relevance, as they play functional roles in obesity-induced insulin resistance, inflammation, and responses to infection. Here, we tested the hypothesis that high-fat-diet (HFD)-induced obesity could impair the mitochondrial respiration of intact and permeabilized splenic CD19+ B cells isolated from C57BL/6J mice and activated ex vivo with lipopolysaccharide (LPS). High-resolution respirometry was used with intact and permeabilized cells. To reveal potential mechanistic targets by which HFD-induced obesity dysregulates B cell mitochondria, we conducted proteomic analyses and 3D serial block face scanning electron microscopy (SBFEM). High-resolution respirometry revealed that intact LPS-stimulated B cells of obese mice, relative to controls, displayed lower ATP-linked, as well as maximal uncoupled, respiration. To directly investigate mitochondrial function, we used permeabilized LPS-stimulated B cells, which displayed increased H2O2 emission and production with obesity. We also examined oxidative phosphorylation efficiency simultaneously, which revealed that oxygen consumption and ATP production were decreased in LPS-stimulated B cells with obesity relative to controls. Despite minimal changes in total respiratory complex abundance, in LPS-stimulated B cells of obese mice, three of the top ten most downregulated proteins were all accessory subunits of respiratory complex I. SBFEM showed that B cells of obese mice, compared to controls, underwent no change in mitochondrial cristae integrity but displayed increased mitochondrial volume that was linked to bioenergetic function. Collectively, these results establish a proof of concept that HFD-induced obesity dysregulates the mitochondrial bioenergetic metabolism of activated splenic B cells.
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