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Expression data from bone marrow macrophage derived from lean and obese mice after 1,4, and 24h exposition to P.gingivalis

ABSTRACT: Obesity is a chronic inflammatory disease that weakens macrophage innate immune response to infections. Since M1 polarization is crucial during acute infectious diseases, we hypothesized that diet-induced obesity inhibits M1 polarization of macrophages in the response to bacterial infection. Using a computational approach in conjunction with microarray data, we identified switching genes that may differentially control the behavior of response pathways in macrophages from lean and obese mice. Bone marrow macrophages (BMMM-NM-&) from lean and obese mice were exposed to live Porphyromonas gingivalis (P. gingivalis) for three incubation times (1 h, 4 h and 24 h). cDNA from BMMM-NM-& of lean and obese mice were hybridized on Affymetrix Mouse Genome 430 2.0 Arrays. Hybridization was performed on three replicates at each time point (18 arrays total).

ORGANISM(S): Mus musculus

SUBMITTER: Salomon Amar

PROVIDER: E-GEOD-47414 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from bone marrow macrophage derived from lean and obese mice after 1,4, and 24h exposition to P.gingivalis

Project description:Obesity is a chronic inflammatory disease that weakens macrophage innate immune response to infections. Since M1 polarization is crucial during acute infectious diseases, we hypothesized that diet-induced obesity inhibits M1 polarization of macrophages in the response to bacterial infection. Using a computational approach in conjunction with microarray data, we identified switching genes that may differentially control the behavior of response pathways in macrophages from lean and obese mice.

2013-06-12 | GSE47414 | GEO

Acetylation and phosphorylation changes to cardiac proteins in experimental HFpEF due to metabolic risk reveal targets for treatment

Project description:Aims: Despite the high prevalence of heart failure with preserved ejection fraction (HFpEF), the pathomechanisms remain elusive and specific therapy is lacking. Disease-causing factors include metabolic risk, notably obesity. However, proteomic changes in HFpEF are poorly understood, hampering therapeutic strategies. We sought to elucidate how metabolic syndrome affects cardiac protein expression, phosphorylation and acetylation in the Zucker diabetic fatty/Spontaneously hypertensive heart failure F1 (ZSF1) rat HFpEF model, and to evaluate some changes regarding their potential for treatment. Main methods: ZSF1 obese and lean rats were fed a Purina diet up to the onset of HFpEF in the obese animals. We quantified the proteome, phosphoproteome and acetylome of ZSF1 obese versus lean heart tissues by mass spectrometry and singled out targets for site-specific evaluation. Key findings: We found the acetylome of ZSF1 obese versus lean hearts more severely altered (21% of proteins changed) than the phosphoproteome (9%) or proteome (3%). Proteomic alterations, confirmed by immunoblotting, indicated low-grade systemic inflammation and endothelial remodeling in obese hearts, but low nitric oxide-dependent oxidative/nitrosative stress. Altered acetylation in ZSF1 obese hearts mainly affected pathways important for metabolism, energy production and mechanical function, including hypo-acetylation of mechanical proteins but hyper-acetylation of proteins regulating fatty acid metabolism. Hypo-acetylation and hypo-phosphorylation of elastic titin in ZSF1 obese hearts explained myocardial stiffening. Significance: Cardiometabolic syndrome alters posttranslational modifications, notably acetylation, in experimental HFpEF. Pathway changes implicate a HFpEF signature of low-grade inflammation, endothelial dysfunction, metabolic and mechanical impairment, and suggest titin stiffness and mitochondrial metabolism as promising therapeutic targets.

2022-10-12 | PXD036259 | Pride

Expression data from human macrophages treated with Porphyromonas gingivalis and its components

Project description:Periodontitis is the most common human infection affecting tooth-supporting structures. It was shown to play a role in aggravating atherosclerosis. To deepen our understanding of the pathogenesis of this disease, we exposed human macrophages to an oral bacteria Porphyromonas gingivalis (P. gingivalis) either as live bacteria, or its lipopolysaccharide (LPS) or fimbria. Microarray data from treated macrophages or control cells were analyzed to define molecular signatures. We focused our analysis on three important groups of genes. Group PG (genes differentially expressed by live bacteria only); Group LFG (genes differentially expressed in response to exposure to LPS and/or FimA); Group CG (core gene set jointly activated by all 3 stimulants). A total of 842 macrophage genes were differentially expressed in at least one of the three conditions compared to naÃ¯ve cells. Using pathway analysis, we found that group CG activates the initial phagocytosis process and induces genes relevant to immune response, whereas group PG can de-activate the phagocytosis process associated with phagosome-lysosome fusion. LFG mostly affected RIG-I-like receptor signaling pathway. 12 samples in total. 4 conditions (treatment with live P. gingivalis, P. gingivalis LPS, P. gingivalis fimbriae, or saline) were used, and triplicates were performed for each condition. We considered the following comparisons: PG vs. Control (saline), PG-LPS vs. Control, and PG-fimbriae vs. Control. Fold-change > 2.0 and FDR < 0.25 were used to select significantly expressed genes.

2010-10-23 | E-GEOD-24897 | biostudies-arrayexpress

Expression data from mouse adipose tissue macrophage

Project description:In mammals, expansion of adipose tissue mass induces accumulation of adipose tissue macrophages (ATMs). We isolated CD11c- (FB) and CD11c+ (FBC) perigonadal ATMs from SVCs of lean (C57BL/6J Lep +/+) and obese leptin-deficient (C57BL/6J Lep ob/ob) mice. We used expression microarrays to generate transcription profiles of perigonadal ATMs from lean (C57BL/6J Lep +/+) and obese (C57BL/6J Lep ob/ob) mice. Profiling purified FBs and FBCs, we identified 521 transcripts whose expression was differentially (nominal p-value < 0.01) expressed between FBs from lean and obese mice and 1509 genes whose expression was differentially (nominal p-value <0.01) expressed between FBC from lean and obese mice RNA was isolated from sorted FBC (F4/80+, CD11b+, CD11c+) cells and FB ( F4/80+, CD11b+, CD11c-) cells and using RNeasy micro-kits (Qiagen), using a PicoPure RNA isolation kit then amplified two-rounds. Labeled cRNA Mouse Genome 430 2.0 arrays (purified FB and FBC adipose tissue macrophages. There was a total of sixteen samples. FB and FBC populations were isolated from 4 lean and 4 obese mice.

2013-12-18 | E-GEOD-53403 | biostudies-arrayexpress

Adipocyte-derived Exosomal miRNAs from Subcutaneous Adipose Tissue: A Novel Mechanism for Obesity-Related Disease

Project description:Affymetrix miRNA 3.0 array profiling of adipocyte-derived exosomes from obese and lean human subjects. We used miRNA arrays to profile exosomes shed from obese and lean human subcutaneous fat that was cultured for 60 minutes. Human obese and lean subcutaneous fat were surgically acquired, dissected, and promptly cultured for 60 minutes. We used the culture supernatants for exosome purification and isolation using ExoQuick-TC Precipitation Solution.

2017-05-15 | E-GEOD-68885 | biostudies-arrayexpress

Adipocyte-derived Exosomal miRNAs: A Novel Mechanism for Obesity-Related Disease

Project description:Affymetrix miRNA 3.0 array profiling of adipocyte-derived exosomes from obese and lean human subjects We used miRNA arrays to profile exosomes shed from obese and lean human visceral and subcutaneous fat that was cultured for 60 minutes. Human obese and lean visceral and subcutaneous fat were surgically acquired, dissected, and promptly cultured for 60 minutes. We used the culture supernatants for exosome purification and isolation using ExoQuick-TC Precipitation Solution

2015-03-03 | E-GEOD-50574 | biostudies-arrayexpress

Targeting mitochondrial reactive oxygen species alleviates allergic airway disease in a mouse model of obese allergic asthma

Project description:Obesity is associated with severe, difficult to control asthma, and increased airway oxidative stress. Mitochondrial reactive oxygen species (mROS) are an important source of oxidative stress leading us to hypothesize that targeting mROS in obese allergic asthma might be an effective treatment strategy. Using a mouse model of house dust mite (HDM) induced allergic airway disease in mice fed a low- (LFD) or high-fat diet (HFD), and the mitochondrial antioxidant MitoQuinone (MitoQ); we investigated the effects of obesity and mROS on airway inflammation, remodelling and airway hyperreactivity (AHR). HDM induces airway inflammation, remodelling and hyperreactivity in both lean and obese mice. Obese allergic mice showed increased lung tissue eotaxin levels, airway tissue eosinophilia and AHR when compared to lean allergic mice. MitoQ reduced markers of airway inflammation, remodelling and hyperreactivity in both lean and obese allergic mice, and tissue eosinophilia in obeseHDM mice. mROS regulates cell signalling by protein oxidation of multiple downstream targets: MitoQ reduced HDM-induced cysteine-sulfenylation of several proteins including those involved in the unfolded protein response (UPR). In summary, mROS mediates the development of allergic airway disease and hence MitoQ might be effective for the treatment for asthma, and specific features of obese asthma.

2023-06-02 | PXD029715 | Pride

Porphyromonas gingivalis gene expression during co-culture with Treponema denticola

Project description:Porphyromonas gingivalis and Treponema denticola are periodontalpathogens that are associated with the severity and progression of periodontal diseases. This study investigates the gene expression of Porphyromonas gingivalis during co-culture with Treponema denticola

2014-03-31 | E-MTAB-2214 | biostudies-arrayexpress

Treponema denticola gene expression during co-culture with Porphyromonas gingivalis

Project description:Porphyromonas gingivalis and Treponema denticola are periodontalpathogens that are associated with the severity and progression of periodontal diseases. this study investigates the gene expression of Treponema denticola during co-culture with Porphyromonas gingivalis.

2014-03-31 | E-MTAB-2257 | biostudies-arrayexpress

A phosphoproteomic analysis of platelets in severe obesity uncovers platelet reactivity and signaling pathways alterations

Project description:Objective: Obesity is associated with a pro-inflammatory and pro-thrombotic state that supports atherosclerosis progression. The goal of this study was to gain insights into the phosphorylation events related to platelet reactivity in obesity and identify platelet biomarkers and altered activation pathways in this clinical condition. Approach and Results: We performed a comparative phosphoproteomic analysis of resting platelets from obese patients and their age- and gender-matched lean controls. The phosphoproteomic data were validated by mechanistic, functional and biochemical assays. We identified 220 differentially regulated phosphopeptides, from at least 175 proteins; interestingly all were up-regulated in obesity. Most of the altered phosphoproteins are involved in Src-family kinases (SFKs)-related signaling pathways, cytoskeleton reorganization and vesicle transport, some of them validated by targeted mass spectrometry. To confirm platelet dysfunction, flow cytometry assays were performed in whole blood indicating higher surface levels of glycoprotein (GP) VI and C-type lectin-like (CLEC) -2 in platelets from obese patients correlating positively with BMI. ROC curves analysis suggested a much higher sensitivity for GPVI to discriminate between obese and lean individuals. Indeed, we also found that obese platelets displayed more adhesion to collagen-coated plates. In line with the above data, sGPVI levels - indicative of higher GPVI signaling activation - were almost double in plasma from obese patients. Conclusion: Our results provide novel information on platelet phosphorylation changes related to obesity, revealing the impact of this chronic pathology on platelet reactivity and pointing towards the main signaling pathways dysregulated.

2022-02-23 | PXD020204 | Pride

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