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Apolipoprotein E deficiency potentiates macrophage resistance to staphylococcus aureus osteomyelitis via regulating cholesterol metabolism

ABSTRACT: Apolipoprotein E deficiency potentiates macrophage resistance to staphylococcus aureus osteomyelitis via regulating cholesterol metabolism

PROVIDER: PRJNA945443 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23881223_1.fastq.gz	Fastqsanger.gz
	SRR23881223_2.fastq.gz	Fastqsanger.gz
	SRR23881224_1.fastq.gz	Fastqsanger.gz
	SRR23881224_2.fastq.gz	Fastqsanger.gz
	SRR23881225_1.fastq.gz	Fastqsanger.gz

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Apolipoprotein E deficiency potentiates macrophage resistance to staphylococcus aureus osteomyelitis via regulating cholesterol metabolism

Project description:To explore how APOE functions in the mechanism of regulation of cholesterol metabolism during S. aureus osteomyelitis, we established S. aureus osteomyelitis models in WT mice and APOE knockout mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of bone marrow from mice mentioned above at day 7 after operation.

2023-07-09 | GSE227521 | GEO

Apolipoprotein E deficiency potentiates macrophage against <i>Staphylococcus aureus</i> in mice with osteomyelitis via regulating cholesterol metabolism.

Project description:IntroductionStaphylococcus aureus (S. aureus) osteomyelitis causes a variety of metabolism disorders in microenvironment and cells. Defining the changes in cholesterol metabolism and identifying key factors involved in cholesterol metabolism disorders during S. aureus osteomyelitis is crucial to understanding the mechanisms of S. aureus osteomyelitis and is important in designing host-directed therapeutic strategies.MethodsIn this study, we conducted in vitro and in vivo experiments to define the effects of S. aureus osteomyelitis on cholesterol metabolism, as well as the role of Apolipoprotein E (ApoE) in regulating cholesterol metabolism by macrophages during S. aureus osteomyelitis.ResultsThe data from GSE166522 showed that cholesterol metabolism disorder was induced by S. aureus osteomyelitis. Loss of cholesterol from macrophage obtained from mice with S. aureus osteomyelitis was detected by liquid chromatography-tandem mass spectrometry(LC-MS/MS), which is consistent with Filipin III staining results. Changes in intracellular cholesterol content influenced bactericidal capacity of macrophage. Subsequently, it was proven by gene set enrichment analysis and qPCR, that ApoE played a key role in developing cholesterol metabolism disorder in S. aureus osteomyelitis. ApoE deficiency in macrophages resulted in increased resistance to S. aureus. ApoE-deficient mice manifested abated bone destruction and decreased bacteria load. Moreover, the combination of transcriptional analysis, qPCR, and killing assay showed that ApoE deficiency led to enhanced cholesterol biosynthesis in macrophage, ameliorating anti-infection ability.ConclusionWe identified a previously unrecognized role of ApoE in S. aureus osteomyelitis from the perspective of metabolic reprogramming. Hence, during treating S. aureus osteomyelitis, considering cholesterol metabolism as a potential therapeutic target presents a new research direction.

| S-EPMC10387542 | biostudies-literature

Biphasic effects of pleiotropic cytokine IL-27 during Staphylococcus aureus implant-associated osteomyelitis

Project description:We aimed to elucidate the mechanism of IL-27/ IL-27 receptor signaling effects on S. aureus osteomyelitis via gene expression studies.

2021-03-16 | GSE168896 | GEO

Mitochondrial Apolipoprotein MIC26 is a metabolic rheostat regulating central cellular fuel pathways

Project description:A variety of metabolic disorders are aggravated by obesity. Since mitochondria play key roles in various catabolic and anabolic reactions encompassing lipid metabolism, optimal functioning of mitochondria is critical in preventing various pathologies. Increased amounts of the apolipoprotein O /MIC26 were found in diabetic patients along with lipid accumulation in murine liver upon MIC26 expression. MIC26 is a MICOS complex constituent present in the mitochondrial inner membrane. The functional interplay between MIC26 and cellular metabolome is not understood. Therefore, we employed a multi-omics approach in WT and MIC26 knockout HepG2 cellular models in normoglycemic and hyperglycemic conditions, along with a variety of functional assays. We found that MIC26 is necessary for maintaining glycolysis and lipid metabolism via CPT1A along with cholesterol synthesis in a nutrient-dependent manner. MIC26 deletion led to metabolic rewiring of glutamine utilisation leading us to propose that mitochondrial ultrastructure and cellular metabolome are functionally interdependent.

2023-12-01 | GSE248848 | GEO

osteomyelitis

Project description:High-resolution transcriptomic analysis of the adaptive response of Staphylococcus aureus during acute and chronic phases of osteomyelitis infection

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CUX1 deficiency potentiates RAS signaling to drive malignancy

Project description:CUX1 deficiency potentiates RAS signaling to drive malignancy

| PRJNA678951 | ENA

Naked mole rat cells are protected from cellular senescence via Wnt/β-catenin-promoted cholesterol metabolism

Project description:The naked mole rat (NMR; Heterocephalus glaber) exhibits cancer resistance and an exceptionally long lifespan of approximately 30 years. The longevity of the NMR is widely debated, as it poses challenges to theories associated with aging, cancer, and redox homeostasis. In the present study, we report unique mechanisms of cholesterol metabolism in NMR cells that could be responsible in part for their anti-senescent properties. We found that NMR fibroblasts abundantly express β-catenin, and that increased β-catenin activity is linked to increased accumulation of cholesterol-enriched lipid droplets. Either β-catenin knockdown or inhibition of cholesterol synthesis abolished lipid droplet formation, and enhanced induction of senescence-like phenotypes. Analysis of β-catenin-regulated genes revealed that β-catenin upregulated the LXR/RXR pathway and Apolipoprotein F, which are involved in cholesterol biogenesis and transport. Specifically, Apolipoprotein F is involved in the accumulation of lipid droplets, protecting NMR cells from cellular senescence. We thus suggest that increased β-catenin activity evolved in NMRs to offset senescence via the accumulation of cholesterol-enriched lipid droplets. Hence, the anti-senescence effects of the Wnt/β-catenin signaling in NMRs reveals new strategies for the development of anti-cancer and anti-aging treatments.

2021-02-21 | GSE147871 | GEO

Apolipoprotein A1-Manipulated Cholesterol Efflux Subverts the Phagocytic Fragility of TAMs and Improves Oncolytic Viro-Immunotherapy in Glioblastoma

Project description:Apolipoprotein A1-Manipulated Cholesterol Efflux Subverts the Phagocytic Fragility of TAMs and Improves Oncolytic Viro-Immunotherapy in Glioblastoma

| PRJNA833879 | ENA

Neuronal γ-secretase regulates lipid metabolism, linking cholesterol to synaptic dysfunction in Alzheimer's disease

Project description:Presenilin mutations that alter γ-secretase activity cause familial Alzheimer's disease (AD), whereas ApoE4, an apolipoprotein for cholesterol transport, predisposes to sporadic AD. Both sporadic and familial AD feature synaptic dysfunction. Whether γ-secretase is involved in cholesterol metabolism and whether such involvement impacts synaptic function remains unknown. Here, we show that in human neurons, chronic pharmacological or genetic suppression of γ-secretase increases synapse numbers but decreases synaptic transmission by lowering the presynaptic release probability without altering dendritic or axonal arborizations. In search of a mechanism underlying these synaptic impairments, we discovered that chronic γ-secretase suppression robustly decreases cholesterol levels in neurons but not in glia, which in turn stimulates neuron-specific cholesterol-synthesis gene expression. Suppression of cholesterol levels by HMG-CoA reductase inhibitors (statins) impaired synaptic function similar to γ-secretase inhibition. Thus, γ-secretase enables synaptic function by maintaining cholesterol levels, whereas the chronic suppression of γ-secretase impairs synapses by lowering cholesterol levels.

2023-08-06 | GSE206102 | GEO

Exhaustion-associated cholesterol deficiency dampens the cytotoxic arm of antitumor immunity

Project description:The concept of targeting cholesterol metabolism to treat cancer has been widely tested in clinics but the benefits are modest, calling for a complete understanding of cholesterol metabolism of intratumoral cells. Low cholesterol levels inhibit T-cell proliferation and cause autophagy mediated apoptosis, particularly for cytotoxic T cells. In the tumor microenvironment, oxysterols mediate reciprocal alterations of the LXR and SREBP2 pathways to cause cholesterol deficiency of T cells, subsequently leading to aberrant metabolic and signaling pathways that drive T cell exhaustion/dysfunction. LXR depletion in CAR-T cells led to improved antitumor function against solid tumor.

2023-04-13 | GSE229611 | GEO

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