Proteomic analysis of the molecular targets of Luteolin in reducing DEHP accumulation in the liver
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Thermo Fisher Scientific instrument model
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): Hepatocyte, Liver, Cell Culture
SUBMITTER: 
Huiting Wang
LAB HEAD: SiYu Chen
PROVIDER: PXD055165 | Pride | 2024-10-25
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Database.rar | Other | |||
| P20211205927_DEHP_1.raw | Raw | |||
| P20211205927_DEHP_2.raw | Raw | |||
| P20211205927_DEHP_3.raw | Raw | |||
| P20211205927_E_LUT_1.raw | Raw |
Items per page: 5 1 - 5 of 8 |
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Project description:Chromatin acetylation is attributed with distinct functional relevance with respect to gene expression in normal and diseased conditions thereby leading to a topical interest in the concept of epigenetic modulators and therapy. We report here the identification and characterization of the acetylation inhibitory potential of an important dietary flavonoid, luteolin. Luteolin was found to inhibit p300 acetyltransferase with competitive binding to the acetyl CoA binding site. Luteolin treatment in a xenografted tumor model of head and neck squamous cell carcinoma (HNSCC), led to a dramatic reduction in tumor growth within 4 weeks corresponding to a decrease in histone acetylation. Cells treated with luteolin exhibit cell cycle arrest and decreased cell migration. Luteolin treatment led to an alteration in gene expression and miRNA profile including up-regulation of p53 induced miR-195/215, let7C; potentially translating into a tumor suppressor function. It also led to down-regulation of oncomiRNAs such as miR-135a, thereby reflecting global changes in the microRNA network. Furthermore, a direct correlation between the inhibition of histone acetylation and gene expression was established using chromatin immunoprecipitation on promoters of differentially expressed genes. A network of dysregulated genes and miRNAs was mapped along with the gene ontology categories, and the effects of luteolin were observed to be potentially at multiple levels: at the level of gene expression, miRNA expression and miRNA processing. Cells treated with luteolin exhibit cell cycle arrest and decreased cell migration. Luteolin treatment led to an alteration in gene expression and mRNA profile
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Project description:Our aim was to identify genes that were differentially expressed in microglia stimulated with Lipopolysaccharide, Luteolin, or both. Affymetrix microarrays were used to analyze RNA samples Experiment Overall Design: RNA from control BV-2 cells, and cells treated for 24h with LPS, Luteolin, or LPS+Luteolin was analyzed with Affymetrix GeneChip Mouse Genome 430 2.0 Arrays. Biological triplicates were analyzed for each condition
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Project description:BACKGROUND: Phthalates are manmade industrial additives used mostly as plasticizers. In addition to their deleterious effects on male genital development, population studies have recently documented correlations between phthalates exposure and subtle impacts on reproductive tract development and on the metabolic syndrome in male adults. In mature rodents liver di-(2-ethylhexyl)-phthalate (DEHP) activates the peroxisome proliferators-activated receptor (PPARalpha), a member of the nuclear receptor (NR) superfamily. OBJECTIVES: Using a systems biology approach, we aimed at defining potential mechanisms underlying the impacts of DEHP on adult mouse liver and testis. METHODS: Thus, we performed a parallel analysis of transcript and metabolic profiles in the liver from adult mice exposed to varying DEHP doses. Moreover, we obtained pangenomic mRNA profiles of laser-captured Leydig and Sertoli cells from mature animals exposed to DEHP. RESULTS: Hepatic genes modulated by DEHP are predominantly PPARalpha targets. However, the induction of some prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways. Integration of hepatic transcriptomic and metabonomic profiles further revealed a correlation between the impacts of DEHP on a cluster of genes and metabolites linked to heme synthesis and on a cluster of Rev-erbalpha target genes related to metabolic and circadian clock pathways. Cell-specific effects of DEHP were investigated in the adult testis and a noticeable impact of DEHP was observed on Leydig cells transcriptome. CONCLUSIONS: We report a detailed analysis of DEHP interference with hepatic Constitutive Androstane Receptor (CAR) and Rev-erbalpha pathways and a novel transcriptional impact of DEHP on adult endocrine cells of the testis. Experiment Overall Design: two condition experiment, Sertoli cells-rich areas from DEHP-treated mice vs. Sertoli cells-rich areas from vehicle-treated mice. Biological replicates: 4 DEHP-treated samples and 4 vehicle-treated samples. Dye-swap design. N=4 DEHP-treated vs vehicle-treated x 2 microarrays (dye-swap)=8 microarrays
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2023-12-01 | GSE219241 | GEO
Project description:The flavonoid luteolin possess a variety of anti-inflammatory properties, but little has known about the detailed mechanisms linked to the anti-metabolic syndrome action of luteolin based on the integration of the transcriptional profile and the phenotype biomarkers. The aim of this study was to investigate the protective role of luteolin on inflammation-mediated metabolic diseases, focusing on its role in modulating toll-like receptor (TLR) signaling pathway triggered up-regulation of pro-inflammatory cytokines. Above all, it provides novel insights into the effect of luteolin on the link among adiposopathy, insulin resistance, hepatic steatosis and fibrosis. C57BL/6J mice were fed a normal, high-fat, and high-fat + 0.005% (w/w) luteolin diet for 16 weeks. In this study, (a) luteolin treatment resulted in an improvement in chronic low-grade inflammation by modulating TLR-signaling pathway resulting in reduced pro-inflammatory cytokines and macrophage accumulation; (b) there is a positive relationship of TLR5, MKK4/7, p38 and JNK-related gene expressions and lipogenesis in luteolin-treated obese mice, which is linked to an attenuation of hepatic lipotoxicity with an increased hepatic anti-oxidant system; (c) luteolin prevented hepatic and adipocyte fibrosis by decreasing ECM accumulation and cathepsin gene expressions; (d) Emr1 and Ccl7 genes, important markers inducing low-grade inflammation, are affected by advancing age as well as body weight, and luteolin treatment normalized those gene expressions; (e) luteolin treatment improved insulin resistance by normalizing pancreatic islet dysfunction, and differentially modulating the plasma GLP-1 and GIP levels. Taken together, luteolin ameliorates the deleterious effects of diet-induced obesity and its comorbidity.
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