Modification of miRNA profile in Caco-2 cells by dietary lipids
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Lidia Daimiel-Ruiz
PROVIDER: E-GEOD-59153 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The effect of CLA on gene expression in Caco-2 cells Experiment Overall Design: Caco-2 cells were treated with linoleic acid (LA; the parent and control fatty acid) trans-10, cis-12 CLA or cis-9, trans-11 CLA for 12 d.
2008-06-14 | E-GEOD-6518 | biostudies-arrayexpress
Project description:For a long time, the BARD1 (BRCA1-associated RING domain 1) protein has been considered as a BRCA1 (BReast Cancer susceptibility gene 1, early onset) interactor, and tumor suppressor mutated in breast and ovarian cancers. Despite its functions in a stable heterodimer with BRCA1, there is increasing evidence for BRCA1-independent functions of BARD1. Here, we investigated BARD1 expression and function in human acute myeloid leukemias and their modulation by epigenetic mechanisms and microRNA. We show that the HDACi (histone deacetylase inhibitor) Vorinostat reduces BARD1 mRNA levels by increasing miR-19a and miR-19b expression levels. Moreover, we identify specific BARD1 isoforms that might act as tumor diagnostic and prognostic markers. Two-condition experiment: untreated NB4 cells (control) vs. NB4 cells treated with 5M-BM-5M SAHA (Vorinostat) for 6h. Biological replicates: 3 control, 3 treated, independently grown and harvested at 6 hours. One replicate per array.
2014-12-22 | E-GEOD-37374 | biostudies-arrayexpress
Project description:The effect of CLA on gene expression in Caco-2 cells Keywords: Human
2007-12-13 | GSE6518 | GEO
Project description:Background & Aims: Non-alcoholic fatty liver disease accompanies obesity and is independently associated with cardiovascular disease. Omega-3 fatty acids, such as docosahexaenoic (DHA) and eicosapentaenoic (EPA) acid, reduce the risk of cardiovascular disease due to their anti-inflammatory and hypolipidemic effects. Recent data suggested that metabolic effects of EPA/DHA as marine phospholipids could be stronger than triglycerides (fish oil). We characterised the mechanisms underlying beneficial effects of EPA/DHA phospholipids alone or in combination with antidiabetic drugs on hepatosteatosis in dietary obese mice. Methods: Male C57BL/6N mice were fed for 7 weeks a corn oil-based high-fat diet (cHF) or subjected to cHF-based interventions: (i) cHF with DHA/EPA as phosphatidylcholine-rich concentrate replacing ~10 % of dietary lipids (PC); ii) cHF with a low-dose of thiazolidinedione rosiglitazone (10 mg/kg diet), which retains some of the beneficial effects but also potentiates hepatic lipid accumulation (R); and iii) PC+R. Metabolic profiling together with hepatic gene expression and lipidomic analyses were performed. Results: PC and PC+R prevented weight gain and glucose intolerance induced by cHF, while all interventions reduced abdominal fat and plasma triglycerides. In contrast to R, PC and PC+R lowered hepatic and plasma cholesterol and eliminated hepatosteatosis. Hepatic microarray analysis primarily revealed a complex downregulation of lipogenic and cholesterol biosynthesis pathways by PC. Lipidomic analysis identified arachidonic acid, DHA and EPA in hepatic phosphatidylcholine and phosphatidylethanolamine fractions as the most important variables. Importantly, down-regulation of genes within these pathways was enlarged by phospholipid versus triglyceride forms of EPA/DHA in an independent experiment. Conclusions: Obesity-associated hepatosteatosis and hypercholesterolemia were ameliorated by marine phospholipids in association with a complex inhibition of biosynthetic pathways in liver. Stronger effects of phospholipids versus triglyceride form of EPA/DHA suggest their preferential use in the prevention and possible treatment of obesity-associated metabolic hepatic dysfunctions.
2014-07-30 | GSE45235 | GEO
Project description:Under caloric restriction, bone marrow adipocytes (BM-Ad) do not decrease in size conversely to white adipocytes, suggesting their unique metabolic properties. We compared human primary BM-Ad with paired subcutaneous adipocytes (SC-Ad) using proteomic and lipidomic approaches. We found that while SC-Ad and BM-Ad share similar morphological features, they possess distinct lipid metabolism. BM-Ad shows enrichment in proteins involved in cholesterol metabolism correlating with increased free cholesterol content while proteins involved in lipolysis were downregulated. In particular, monoacylglycerol lipase expression was strongly reduced in BM-Ad, leading to accumulation of monoacylglycerol. Consequently, basal and induced lipolytic responses were absent in BM-Ad, affirming their differences in metabolic fitness upon caloric restriction. These specific metabolic features are not recapitulated in vitro using common protocols to differentiate bone marrow mesenchymal stem cells. Thus, contrary to classical SC-Ad, BM-Ad display a specific lipid metabolism, as they are devoid of lipolytic activity and exhibit a cholesterol-orientated metabolism.
2020-01-29 | PXD016322 | Pride
Project description:Micro-RNA associated with low-N tolerance have been identified in rice (Oryza sativa) genotypes on the basis of differential expression of miRNA in low-N tolerant and low-N sensitive genotypes of rice. Since, miRNAs emerged as key players in plant responses and adaptation to stress, identification of low-N responsive miRNAs and their targets could help to uncover the molecular mechanisms of N-deficiency tolerance in plants. We used affymetrix based GeneChip miRNA_2.0 Array to detail the global programme of miRNA expression variation in low-N tolerant (IC-547557) and low -N sensitive (Vivek Dhan). Low-N tolerant and low-N sensitive rice genotypes were grown using the nutrient medium containing 2 mM K2SO4, 2 mM MgSO4, 1 mM CaCl2, 0.3 mM NaH2PO4, 40 M-BM-5M Fe-EDTA, 9 M-BM-5M MnCl2, 25 M-BM-5M Na2MoO4, 20 M-BM-5M H3BO3, 1.5 M-BM-5M ZnSO4, and 1.5 M-BM-5M CuSO4. The nitrogen in the form of NH4NO3 was maintained as 0.01 mM (low-N condition). The pH of the nutrient solutions was adjusted to 6.0 and the solutions were changed every three days. Twenty-day-old plants were sampled for expression studies of miRNA.
2012-05-24 | E-GEOD-38213 | biostudies-arrayexpress
Project description:Cylindrospermopsin (CYN) is a cyanotoxin that has been recognised as an emerging potential public health risk. Although CYN toxicity has been demonstrated, the mechanisms involved have not been fully characterised. To identify some key pathways related to this toxicity, we studied the transcriptomic profile of human intestinal Caco-2 cells exposed to a sub-toxic concentration of CYN (1.6 M-BM-5M for 24hrs) using a non-targeted approach. CYN was shown to modulate different biological functions which were related to growth arrest (with down-regulation of cdkn1a and uhrf1 genes), and DNA recombination and repair (with up-regulation of aptx and pms2 genes). Our main results reported an increased expression of some histone-modifying enzymes (histone acetyl and methyltransferases MYST1, KAT5 and EHMT2) involved in chromatin remodelling, which is essential for initiating transcription. We also detected greater levels of acetylated histone H2A (Lys5) and dimethylated histone H3 (Lys4), two products of these enzymes. In conclusion, CYN overexpressed proteins involved in DNA damage repair and transcription, including modifications of nucleosomal histones. Our results highlighted some new cell processes induced by CYN. Modulation of gene expression in differentiated Caco-2 cells was measured at 24 hours after exposure to doses of 0 and 1.6 M-BM-5M of cylindrospermopsin. Six independent experiments were performed, but only 11 samples (5 controls and 6 exposed to cylindrospermopsin) had an RNA quality indicator M-bM-^IM-% 9 and were used for the microarray experiments.
2014-03-11 | E-GEOD-55723 | biostudies-arrayexpress
Project description:Dietary polyunsaturated fatty acids (PUFA) act as potent natural hypolipidemics and are linked to many health benefits in humans and in animal models. Mice fed long-term a high fat diet, in which medium-chain alpha linoleic acid (ALA) was partially replaced by long-chain docosahexaenoic (DHA) and eicosapentaenoic (EPA) fatty acids, showed reduced accumulation of body fat and prevention of insulin resistance, besides increased mitochondrial beta-oxidation in white adipose tissue and decreased plasma lipids. ALA, EPA and DHA all belong to PUFA of n-3 series. The intestine is a gatekeeper organ for ingested lipids. To examine the potential contribution of the intestine in the beneficial effects of EPA and DHA, this study assessed gene expression changes using whole genome microarray analysis on small intestinal scrapings. The main biological process affected was lipid metabolism. Fatty acid uptake, peroxisomal and mitochondrial beta-oxidation, and omega-oxidation of fatty acids were all increased. Quantitative real time PCR and intestinal fatty acid oxidation measurements ([14C(U)]-palmitate) confirmed significant gene expression differences in a dose-dependent manner. Furthermore, no major changes in the expression of lipid metabolism genes were observed in colonic scrapings. In conclusion, we show that marine n-3 fatty acids regulate small intestinal gene expression patterns. Since this organ contributes significantly to whole organism energy use, this adaptation of the small intestine may contribute to the complex and observed beneficial physiological effects of these natural compounds under conditions that will normally lead to development of obesity and diabetes. Experiment Overall Design: Male 4-month-old C57BL/6J mice were maintained for 4 weeks on semisynthetic high-fat (20% wt/wt) diets differing in the composition of n-3 PUFA. Two isocaloric diets were used (n=12): control sHFf diet which contained flax-seed oil (rich in ALA) as the only lipid source, or the sHFf-F2 diet, which had the same composition except that 44 % of the lipids were replaced by a n-3 PUFA concentrate (EPA&DHA) containing 6 % EPA and 51 % DHA (EPAX 1050TG; EPAX AS, Lysaker, Norway). Quality control of RNA samples showed that four samples did not pass quality thresholds, and these samples were excluded from array analysis (two control small intestine samples and one EPA&DHA small intestine sample). The remaining RNA samples were pooled per tissue per diet group. Thus; the flax-seed (control) array was hybridized with RNA pooled from of 10 mice, the PUFA array was hybridized with RNA pooled from 11 mice.
2009-04-16 | E-GEOD-11936 | biostudies-arrayexpress
Project description:Objective: Although relationships between smoking and cardiovascular diseases (CVD), and CVD and lipids are established, direct impact of cigarette smoke (CS) on lipidomes remains elusive. We investigated the effect of 6 month smoke exposure on a well-established mouse model for human atherogenesis, Apoe mouse plasma, liver, and aorta molecular lipid profiles and liver transcriptome. // Methods: Plasma, liver, and aorta samples from Apoe mice exposed to CS or fresh air for 6 months were extracted for lipids using robotic-assisted method and analyzed by mass spectrometry. Gene expression of samples from the same livers was obtained on microarrays. Development of atherosclerosis in aorta was further assessed by plaque size measurement in the aortic arch and lipoprotein measurements in plasma and in the plaque. // Results: CS increased most lipid classes and molecular lipid species in tissues evaluated. In plasma, free cholesterol, ceramides, cerebrosides, and majority of phospholipids were increased in CS-exposed mice. In liver, CS elevated several lipid species including free and esterified cholesterol, triacylglycerols, phospholipids, sphingomyelins, and ceramides. In aorta, more than 2-fold higher cholesteryl ester (CE), lysophosphatidylcholine, and glucosyl/galactosylceramide levels were recorded in mice exposed to CS compared to mice exposed to fresh air. Moreover, CS exposure induced a significant decrease in several plasma CE and phosphatidylcholine species that contained polyunsaturated fatty acids. Genes involved in amino acid and lipid metabolism showed perturbed transcription profiles in liver. // Conclusion: These data reveal molecular details accompanying the increase in plaque size, sign of atherogenesis in Apoe mice, which is accelerated by CS exposure.
2013-10-03 | E-MTAB-1195 | biostudies-arrayexpress