Changes in cellular gene expression during prototype foamy virus infection
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE200199 | GEO | 2022/04/08
REPOSITORIES: GEO
Similar Datasets
Project description:Changes in cellular gene expression during prototype foamy virus infection
| PRJNA823659 | ENA
Project description:Macrophages in atherosclerotic aorta are major population in lesion and contributes to lesion formation by becoming foam cells. To investigate in vivo transcriptome profiles of those macrophages, we extracted foamy and non-foamy macrophages from atherosclerotic aorta using lipid probe-based flow cytometry sorting. Our data indicates that intima non-foamy and foamy macrophages show different mRNA expressions. Rather than non-foamy macrophages, foamy macrophages expressed more genes related to cholesterol metabolism, oxidative phosphorylation, lysosome and so on. The non-foamy macrophages expressed more genes related to immune response (Il-1b related pathways, TNF, TLR signaling pathways) than foamy macrophages.
2018-08-30 | GSE116239 | GEO
Project description:Atherosclerosis-associated vascular disease is the leading cause of death worldwide. Clinical and experimental data demonstrated that circulating monocytes internalize plasma lipoproteins and become lipid-laden foamy cells in hypercholesterolemic subjects. This study was designed to identify the endocytic mechanisms responsible for foamy monocyte formation, perform functional and transcriptomic analysis of foamy and non-foamy monocytes, and characterize specific monocyte subsets in the circulation from normocholesterolemic controls and hypercholesterolemic patients. The presence of foamy monocytes was confirmed in hypercholesterolemic mice and humans via flow cytometry analysis. High resolution scanning electron microscopy (SEM) and quantification of FITC/TRITC-dextran internalization demonstrated macropinocytosis stimulation in human (THP-1) and wild type murine monocytes in vitro. Stimulation of macropinocytosis induced foamy monocyte formation in the presence of unmodified, native LDL (nLDL) and oxidized LDL (ox-LDL) in vitro. Genetic blockade of macropinocytosis (LysMCre+ Nhe1f/f) inhibited foamy monocyte formation in hypercholesterolemic mice in vivo and attenuated monocyte adhesion to atherosclerotic aortas ex vivo. qRT-PCR quantified mRNA levels of major scavenger receptors (SR) in foamy and non-foamy monocytes and identified CD36 as a major SR increasing in response to lipid loading. Deletion of CD36 (Cd36-/-) inhibited foamy monocyte formation in hypercholesterolemic mice. Mechanistic studies identified NADPH oxidase 2 (Nox2)-derived superoxide (O2⋅−) as an important downstream signaling molecule stimulating macropinocytosis in monocytes. Bulk RNA-sequencing characterized transcriptional differences between non-foamy and foamy monocytes and macrophages. Flow cytometry analysis of CD14 and CD16 expression demonstrated a significant increase in intermediate monocytes in hypercholesterolemic patients compared to normocholesterolemic controls. These results provide novel insights into the mechanisms of foamy monocyte formation and potentially identify new therapeutic targets in the treatment of atherosclerosis.
2024-12-26 | GSE278101 | GEO
Project description:After spinal cord injury (SCI), infiltrating macrophages undergo excessive phagocytosis of myelin and cellular debris, forming lipid-laden foamy macrophages. To understand their role in the cellular pathology of SCI, investigation of foamy macrophage phenotype in vitro revealed a unique inflammatory profile, increased reactive oxygen species (ROS) production, and mitochondrialdysfunction. Bioinformatic analysis identified PI3K as a regulator of inflammation in foamy macrophages, and pharmacological inhibition of this pathway decreased lipid content and inflammatory cytokine and ROS production in these cells. Macrophage-specific inhibition of PI3K using liposomes significantly decreased foamy macrophages at the injury site after a mid-thoracic contusive SCI in mice. RNA sequencing and in vitro analysis of foamy macrophages revealed increased autophagy after PI3K inhibition as a potential mechanism for reduced cellular lipid accumulation. Together, our data suggest that formation of pro-inflammatory foamy macrophages after SCI is due to activation of PI3K signaling that leads to decreased autophagy.
2023-12-05 | GSE237511 | GEO
Project description:Untreated or 20 J/m2 UVC treated RKO cells were collected and RNA from either whole-cell lysates or from polysomal fractions was extracted at 0 (untreated), 3, 6, and 12 h after treatment. RNA from whole-cell lysates or each of 11 polysomal fraction was reverse-transcribed in the presence of [α-33P]dCTP and the radiolabeled product used to hybridize human cDNA arrays. The experiment was repeated using three independent sample sets. The samples were named T-c-A, T-c-B, T-c-C, T-3h-A, T-3h-B, T-3h-C, T-6h-A, T-6h-B, T-6h-C, T-12h-A, T-12h-B, T-12h-C, P-c-1-A, P-c-2-A, P-c-3-A, P-c-4-A, P-c-5-A, P-c-6-A, P-c-7-A, P-c-8-A, P-c-9-A, P-c-10-A, P-c-11-A, P-c-1-B, P-c-2-B, P-c-3-B, P-c-4-B, P-c-5-B, P-c-6-B, P-c-7-B, P-c-8-B, P-c-9-B, P-c-10-B, P-c-11-B, P-c-2-C, P-c-3-C, P-c-4-C, P-c-5-C, P-c-6-C, P-c-7-C, P-c-8-C, P-c-9-C, P-c-10-C, P-c-11-C, P-3h-1-A, P-3h-2-A, P-3h-3-A, P-3h-4-A, P-3h-5-A, P-3h-6-A, P-3h-7-A, P-3h-8-A, P-3h-9-A, P-3h-10-A, P-3h-11-A, P-3h-1-B, P-3h-2-B, P-3h-3-B, P-3h-4-B, P-3h-5-B, P-3h-6-B, P-3h-7-B, P-3h-8-B, P-3h-9-B, P-3h-10-B, P-3h-11-B, P-3h-1-C, P-3h-2-C, P-3h-3-C, P-3h-4-C, P-3h-6-C, P-3h-7-C, P-3h-8-C, P-3h-9-C, P-3h-10-C, P-3h-11-C, P-6h-1-A, P-6h-2-A, P-6h-3-A, P-6h-4-A, P-6h-5-A, P-6h-6-A, P-6h-7-A, P-6h-8-A, P-6h-9-A, P-6h-10-A, P-6h-11-A, P-6h-1-B, P-6h-2-B, P-6h-3-B, P-6h-4-B, P-6h-5-B, P-6h-6-B, P-6h-7-B, P-6h-8-B, P-6h-9-B, P-6h-10-B, P-6h-11-B, P-6h-1-C, P-6h-2-C, P-6h-3-C, P-6h-4-C, P-6h-5-C, P-6h-6-C, P-6h-7-C, P-6h-8-C, P-6h-9-C, P-6h-10-C, P-6h-11-C, P-12h-1-A, P-12h-2-A, P-12h-3-A, P-12h-4-A, P-12h-5-A, P-12h-6-A, P-12h-7-A, P-12h-8-A, P-12h-9-A, P-12h-10-A, P-12h-11-A, P-12h-1-B, P-12h-2-B, P-12h-3-B, P-12h-4-B, P-12h-5-B, P-12h-6-B, P-12h-7-B, P-12h-8-B, P-12h-9-B, P-12h-10-B, P-12h-11-B, P-12h-1-C, P-12h-2-C, P-12h-3-C, P-12h-6-C, P-12h-7-C, P-12h-8-C, P-12h-9-C, P-12h-10-C, P-12h-11-C. ‘T’ represents total RNA, ‘P’ represents RNA from polysomes fractions, ‘c’ represents RNA from untreated cells, ‘3h’ represents RNA from cells collected 3 h after UVC treatment, ‘6h’ represents RNA from cells collected 6 h after UVC treatment, ‘12h’ represents RNA from cells collected 12 h after UVC treatment. The numbers 1-11 correspond to the each polysomal fraction. The letters A, B and C correspond to the three independent experimental datasets. Keywords = post-transcriptional / translation / nascent protein synthesis / stress response / ribonomics Keywords: ordered
2004-06-02 | GSE1440 | GEO
Project description:Bulk RNA-seq of foamy and non-foamy intimal macrophages from ApoE -/- mouse
| PRJNA477844 | ENA
Project description:Formation of foam cell macrophages (FCMs), which sequester extracellular modified lipids, is a key event in atherosclerosis. How lipid loading affects macrophage phenotype is controversial, with evidence suggesting either pro- or anti-inflammatory consequences. To investigate this further, we compared the transcriptomes of foamy and non-foamy macrophages (NFMs) that accumulate in the subcutaneous granulomas of fed-fat ApoE null mice and normal chow fed wild-type mice in vivo. Consistent with previous studies, LXR/RXR pathway genes were significantly over-represented among the genes up-regulated in foam cell macrophages. Unexpectedly, the hepatic fibrosis pathway, associated with platelet derived growth factor and transforming growth factor-? action, was also over-represented. Several collagen polypeptides and proteoglycan core proteins as well as connective tissue growth factor and fibrosis-related FOS and JUN transcription factors were up-regulated in foam cell macrophages. Increased expression of several of these genes was confirmed at the protein level in foam cell macrophages from subcutaneous granulomas and in atherosclerotic plaques. Moreover, phosphorylation and nuclear translocation of SMAD2, which is downstream of several transforming growth factor-? family members, was also detected in foam cell macrophages. We conclude that foam cell formation in vivo leads to a pro-fibrotic macrophage phenotype, which could contribute to plaque stability, especially in early lesions that have few vascular smooth muscle cells. Samples (n=4/group): Foam cell macrophages (FCM) isolated from inflammatory sponges placed in ApoE null mice fed a high-fat diet (n=4), non-foamy macrophages (NFM) isolated from inflammatory sponges placed in control mice fed a normal diet (n=4).
2015-07-23 | E-GEOD-70126 | biostudies-arrayexpress
Project description:To investigate the function of Trem2 on foamy macrophage gene regulation, we generated Trem2 deficientBV2 cells using CRISPR and comparedgene expression to Trem2 sufficientcontrols in the presence or absence of cholesterol loading.
2023-05-08 | GSE231659 | GEO
Project description:This study focuses metabolic footprinting of Vero cells infected by Mayaro virus. Nuclear magnetic resonance combined with multivariate analytical methods and tools of pattern recognition shows that metabolic changes can be attributed to the effect of Mayaro virus infection. Vero cells infected by Mayaro and incubated for periods of 2h, 6h and 12h show in each period different variations in the levels of several metabolites such as amino acids, organic acids and carbohydrate. These organic compounds are metabolites involved in the pathway of glycolysis, tricarboxylic acid cycle, pentose phosphate pathway, and the oxidation pathway of fatty acids (via the β-oxidation). This study of footprinting analysis demonstrates the effect of the action of virus in the metabolism of the Vero cells, moreover, these analyses indicate intracellular metabolic state, and contributes to the knowledge of the microorganism influence on cellular metabolism.
2021-10-28 | MTBLS639 | MetaboLights