DHA effect on endothelial cells (HUVEC) under proinflammatory condition
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Rosanna Martinelli
PROVIDER: E-GEOD-57825 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Farmed and wild Atlantic salmon was given either vegetable oil (low DHA and EPA) feed or fish oil (high in DHA and EPA) feed or phospholipid (high in phospholipid) feed from start of feeding. We sampled and RNAseq two tissues (pyloric caeca and liver) on day 0, day 48, day 65 and day 94 after initial feeding.
2019-10-30 | E-MTAB-8306 | biostudies-arrayexpress
Project description:Previously published results from our double-blind, placebo-controlled parallel study with docosahexaenoic acid (DHA) supplementation (3 g/d, 90 d) to hypertriglyceridemic men (39-66yr) showed that DHA reduced several risk factors for cardiovascular disease (CVD), including the plasma concentration of inflammatory markers. To determine the effect of DHA supplementation on the global gene expression pattern, we performed Affymetrix GeneChip microarray analysis of blood cells (treated with lipopolysaccharide (LPS) or vehicle) drawn before and after the supplementation from the hyperlipidemic men who participated in the previous study. Genes that were significantly differentially regulated by the LPS treatment and DHA supplementation were identified. Differential regulation of 18 genes was then confirmed by quantitative RT-PCR. Both microarray and qRT-PCR data showed that the expression of LDL receptor (LDLR), oxidized LDL receptor (OLR1), and cathepsin L1 (CTSL) was significantly suppressed by DHA supplementation; however, LPS stimulated the expression of LDLR and CTSL but not that of OLR1. LPS up-regulated and DHA suppressed the expression of prostaglandin E synthase (PTGES), PPAR delta, and various chemokines. Enrichment with Gene Ontology categories demonstrated that the genes related to transcription factor activity, immune responses, host defense responses, inflammatory responses, and apoptosis were inversely regulated by LPS and DHA. These results provide supporting evidence for the anti-inflammatory effects of DHA supplementation, and reveal previously unrecognized genes that are regulated by DHA, and are associated with risk factors of cardiovascular diseases. Double-blind, placebo-controlled parallel study with DHA supplementation to hypertriglyceridemic men. Gene expression detected in LPS-stimulated (LPS) and unstimulated (vehicle) white blood cells. 3-4 replicates per group.
2010-02-21 | E-GEOD-20114 | biostudies-arrayexpress
Project description:To understand the transcripts regulated by inflammation and how this regulation may differ between different individuals, the transcriptome of HUVECs stimulated with inflammatory mediators was examined in 9 different individuals. In the study present here, HUVEC isolates from 9 different individuals were cultured until passage 4 in fully supplemented growth conditions. Passage 4 HUVEC isolates were then treated with a cocktail of inflammatory mediators (10ng/ml TNF-α, Il-1β, Il-8) for a period of 24 hours prior to RNA extraction. RNA was extracted and hybridised onto CodeLink microarrays. The expression profiles in the inflammatory mediator treated condition were examined along side a superset of the same biological replicates that were untreated (also submitted), to facilitate assessment of the resting transcriptome.
2011-07-19 | E-GEOD-23069 | biostudies-arrayexpress
Project description:We have analyzed the variation of transcriptome of HUVECs intoxicated by the lethal toxin of Bacillus anthracis at 4 and 8 hours Experiment Overall Design: Three experimental conditions with two biological replicates for the control condition corresponding to untreated HUVEC monolayer. RNA were extracted before labeling and hybridizations on Human U133A Plus 2.0 Affymetrix GeneChip
2010-01-29 | E-GEOD-12131 | biostudies-arrayexpress
Project description:Transcriptional profiling of Human Umbilical Vein Endothelial Cells (HUVEC) comparing untreated control cells with IL-1-treated cells with or without pre-treatment with DHA.
2015-05-20 | GSE57825 | GEO
Project description:Background: Docosahexaenoic acid (DHA) is a natural compound with anticancer and anti-angiogenesis activity that is currently under investigation as both a preventative agent and an adjuvant to breast cancer therapy. However, the precise mechanisms of DHA’s anticancer activities are unclear. It is understood that the intercommunication between cancer cells and their microenvironment is essential to tumor angiogenesis. Exosomes are extracellular vesicles that are important mediators of intercellular communication and play a role in promoting angiogenesis. However, very little is known about the contribution of breast cancer exosomes to tumor angiogenesis or whether exosomes can mediate DHA’s anticancer action. Results: Exosomes were collected from MCF7 and MDA-MB-231 breast cancer cells after treatment with DHA. We observed an increase in exosome secretion and exosome microRNA contents from the DHA-treated cells. The expression of 83 microRNAs in the MCF7 exosomes was altered by DHA (>2-fold). The most abundant exosome microRNAs (let-7a, miR-23b, miR-27a/b, miR-21, let-7, and miR-320b) are known to have anti-cancer and/or anti-angiogenic activity. These microRNAs were also increased by DHA treatment in the exosomes from other breast cancer lines (MDA-MB-231, ZR751 and BT20), but not in exosomes from normal breast cells (MCF10A). When DHA-treated MCF7 cells were co-cultured with or their exosomes were directly applied to endothelial cell cultures, we observed an increase in the expression of these microRNAs in the endothelial cells. Furthermore, overexpression of miR-23b and miR-320b in endothelial cells decreased the expression of their pro-angiogenic target genes (PLAU, AMOTL1, NRP1 and ETS2) and significantly inhibited tube formation by endothelial cells, suggesting that the microRNAs transferred by exosomes mediate DHA’s anti-angiogenic action. These effects could be reversed by knockdown of the Rab GTPase, Rab27A, which controls exosome release. Conclusions: We conclude that DHA alters breast cancer exosome secretion and microRNA contents, which leads to the inhibition of angiogenesis. Our data demonstrate that breast cancer exosome signaling can be targeted to inhibit tumor angiogenesis and provide new insight into DHA’s anticancer action, further supporting its use in cancer therapy. Examination of small RNA populations in MCF7 cells and exosomes after DHA treatment.
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Project description:Dihydroxyacetone (DHA) is an attractive molecule produced in a wide range of industries . DHA is found among all the kingdoms as an intermediate of various metabolic pathways and can be used as a carbon source by many organisms. The bacterium Escherichia coli is able to grow on DHA as the sole carbon source albeit at a low growth rate (0.1 h-1). If the topology of DHA metabolic network has been characterized, the function and regulation of the metabolic pathways involved in DHA metabolism remain unsolved. Here, we aimed to better understand DHA metabolism in E. coli BW25113 by exploring its transcriptional pattern on DHA versus glucose. We also studied the pattern of three DHA pathway mutants (dhaKLM, ptsA and glpK).
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Project description:To understand the biological variability that exists between different individuals, the resting (untreated) transcriptome from 15 different individuals was examined. Transcripts expressed in a bimodal manor across the 15 biological replicates were identified for further examination. In the study presented here, HUVEC isolates from 15 different individuals were cultured until passage 4 in fully supplemented growth conditions. RNA was extracted and hybridised onto CodeLink microarrays. The expression profiles in the untreated condition were examined along side a subset of the same biological replicates treated with a cocktail of inflammatory mediators (10ng/ml TNF-α, Il-1β, Il-8) for a period of 24 hours prior to RNA extraction (also submitted).
2011-07-19 | E-GEOD-23068 | biostudies-arrayexpress
Project description:The similar response of endothelial cells to exogenous IL-33 or IL-1M-NM-2 prompted us to compare the genome-wide transcription profile of confluent human umbilical vein endothelial cell (HUVEC) cultures after 4 hours exposure to IL-33 or IL-1M-NM-2. Analysis of these data revealed a striking similarity in the transcriptional response to the two cytokines. Pooled HUVEC from 10 donors were seeded 10.000 cells/cm2 and cultured for 4 days before stimulation for 4 hours with IL-1M-NM-2 0.5 ng/ml or IL-33 50 ng/ml. Total RNA was isolated using the RNeasy Mini Kit (Qiagen) according to instructions of the manufacturer. Microarrays were performed using an Illumina Human6 v2 Expression Beadchip, and the raw data was pre-processed by IlluminaM-bM-^@M-^Ys BeadStudio software V2. The expression service was provided by Helse SM-CM-8r-M-CM-^Xst/University of Oslo Microarray Core Facility, a member of the Norwegian Microarray Consortium supported by the functional genomics program (FUGE) at the Research Council of Norway.
2013-03-05 | E-GEOD-37624 | biostudies-arrayexpress
Project description:Cutaneous melanoma is the most aggressive skin cancer showing high mortality at advanced clinical stages. Platelet-Derived Growth Factor Receptor alpha (PDGFR-alpha) is known to strongly inhibit melanoma and endothelial cells proliferation, in vitro as well in vivo. PDGFR-alpha expression has been found to be reduced in metastatic human melanoma-biopsies, as compared to benign nevi-biopsies, thus implying a negative selection of PDGFR-alpha expressing cells, in melanoma. In the present study PDGFR-alpha was transiently overexpressed in endothelial (HUVEC) and melanoma (SK-Mel-28) human cells; a strong anti-proliferation effect was observed, along with profound effects on mRNA and miRNA expression. In detail, gene-expression profiling showed that PDGFR-alpha over-expression affects the expression of 82 transcripts in HUVEC (41 up-, 41 down-regulated), and 52 Transcripts in SK-Mel-28 (43 up-, 9 down-regulated). Finally, a miRNA profiling showed that 14 miRs are up-regulated and 39 are down-regulated in PDGFR-alpha overexpressing cells. Accurate validation with alternative techniques demonstrated that CXCL10 is one of the most significantly up-regulated at both gene- and protein level, in combination with a strong down-regulation of miR-503 in both HUVEC and SK-Mel-28 overexpressing PDGFR-alpha. We then demonstrate that CXCL10 is a validated miR-503 target, and that the anti-proliferation effect of PDGFR-alpha is reverted by specific CXCL-10 neutralization. In conclusion, PDGFR-alpha overexpression strongly inhibits endothelial- and melanoma- proliferation in a CXCL-10 dependent way, by significantly down-regulating miR-503 expression. This data set contains the results of the mRNA analysis.
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