Immunomodulating effects of 13- and 16-hydroxylated docosahexaenoyl ethanolamide in LPS stimulated RAW264.7 macrophages
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PROVIDER: PRJNA671756 | ENA |
REPOSITORIES: ENA
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Project description:Docosahexaenoyl ethanolamide (DHEA), the ethanolamine conjugate of the n-3 long chain polyunsaturated fatty acid docosahexaenoic acid, is endogenously present in the human circulation and in tissues. Its immunomodulating properties have been (partly) attributed to an interaction with the cyclooxygenase-2 (COX-2) enzyme. Recently, we discovered that COX-2 converts DHEA into two oxygenated metabolites, 13- and 16-hydroxylated-DHEA (13- and 16-HDHEA, respectively). It remained unclear whether these oxygenated metabolites also display immunomodulating properties like their parent DHEA. In the current study we investigated the immunomodulating properties of 13- and 16-HDHEA in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. The compounds reduced production of tumor necrosis factor alpha (TNFα), interleukin (IL)-1β and IL-1Ra, but did not affect nitric oxide (NO) and IL-6 release. Transcriptome analysis showed that the compounds inhibited the LPS-mediated induction of pro-inflammatory genes (InhbA, Ifit1) and suggested potential inhibition of regulators such as toll-like receptor 4 (TLR4), MyD88, and interferon regulatory factor 3 (IRF3), whereas anti-inflammatory genes (SerpinB2) and potential regulators IL-10, sirtuin 1 (Sirt-1), fluticasone propionate were induced. Additionally, transcriptome analysis of 13-HDHEA suggests a potential anti-angiogenic role. In contrast to the known oxylipin-lowering effects of DHEA, liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS) analyses revealed that 13- and 16-HDHEA did not affect oxylipin formation. Overall, the anti-inflammatory effects of 13-HDHEA and 16-HDHEA are less pronounced compared to their parent molecule DHEA. Together, this suggests that the COX-2 metabolism of DHEA may act as a regulatory mechanism to limit the anti-inflammatory properties of DHEA.
2021-02-27 | GSE160086 | GEO
Project description:Translational profiling of RAW264.7 cells stimulated with LPS in the presence and absence of 125ng/ml mycolactone: polysomal and subpolysomal RNA isolated by sucrose gradient centrifugation to determine the effect of mycolactone on translation during a proinflammatory response
2018-03-21 | GSE103002 | GEO
Project description:We sought to characterize the genomic localization of the YEATS domain protein AF9 in the macrophage-like cell line RAW 264.7 +/- LPS stimulation and +/- sodium crotonate pretreatment. We performed chromatin immunoprecipitation followed by massively parallel sequencing (ChIP-seq) for endogenous AF9 or for a FLAG-tagged AF9 transgene in RAW264.7 or a RAW264.7 cell line engineered to express FLAG-AF9, respectively.
2016-04-21 | GSE76539 | GEO
Project description:Unanticipated regulatory protein modifications can be discovered from the unbiased comprehensive analysis of biological systems using SAMPEI. To explore this idea, we sought to map protein modifications induced during mammalian cell differentiation, modeled by the response of mouse RAW264.7 macrophage cells to lipopolysaccharide (LPS), a potent inducer of macrophage activation and differentiation that involves extensive protein and metabolic signaling.
2021-07-22 | PXD019853 | Pride
Project description:Density dependent gene expression change in RAW264.7 cells stimulated without or with LPS.
| PRJNA667842 | ENA
Project description:(1) We sought to characterize the genomic profiles of H3K18Ac and H3K18Cr before and after the activation of the LPS-induced inflamatory response to elucidate the role of differential acylation in the process of gene activation. We performed chromatin Immunoprecipitation followed by massively parallel sequencing (ChIP-seq) with two antibodies, anti-H3K18Ac and anti-H3K18Cr, in RAW264.7 cells +/- LPS stimulation. (2) We also sought to characterize the effect of increasing the cellular concentration of crotonyl-CoA prior to LPS-stimulation on the expression of different classes of LPS-induced genes. We performed RNA-seq on mRNA isolated from RAW264.7 cells under four conditions a) untreated and unstimulated, b) untreated and LPS stimulated, c) crotonate pre-treated and unstimulated, d) crotonate pre-treated and LPS stimulated. Sequencing was performed on the HiSeq2000 (Illumina).
2015-03-26 | GSE63889 | GEO
Project description:Background: Toll-like family of receptors recognizes pathogen-associated molecular patterns (PAMPs) from different organisms. TLR4 is the receptor for bacterial lipopolysaccharide (LPS), dsRNA viral mimic poly(I:C) binds to TLR3, and bacterial CpG DNA signals through TLR9. TLR4 signaling is mediated by adaptor molecules Myd88 and TRIF while TLR3 pathway involves only the TRIF adaptor and TLR9 signals solely through Myd88. Methods: To identify genes other than those in TLR pathways that mediate macrophage response to different PAMPs, RAW264.7 cells were stimulated with LPS, poly(I:C), or CpG DNA, and RNA was profiled on microarrays 6 hrs and 24 hrs post-treatment. Gene expression data were analyzed to determine genes, pathways and transcriptional networks that are in common and unique to each of the three TLR stimuli. Potentially novel candidates revealed by this analysis were tested for their role in innate immunity using RNA interference. Results: Many genes are differentially regulated by LPS and poly(I:C) at both 6 hrs and 24 hrs following treatment, while CpG DNA elicits a much less pronounced transcriptional response. By analyzing gene expression data for networks and pathways, we prioritized differentially expressed genes that are in common to all three PAMPs as well as those shared by LPS and poly(I:C). Knockdown by RNA interference of two genes, Plec1 and TPST1, inhibited production of IL-6 in response to LPS in cultured macrophages. Conclusions: We have identified novel innate immunity genes that may be important in macrophage response to LPS, poly(I:C), and CpG DNA stimuli. Our results provide potential biomarkers and therapeutic targets that should be further investigated in mice and human populations. Keywords: time course For each treatment (Sigma LPS, LIST LPS, and media only), three biological replicates (separate macrophage cultures and RNA isolations) were profiled. Each sample was labeled with Cy3 and Cy5 and co-hybridized with Stratagene Universal Mouse Reference (dye flip techical replicates). Expression at 2 timepoints (6 and 24 hours post-treatment) was assessed.
2010-10-01 | E-GEOD-21548 | biostudies-arrayexpress
Project description:Background: Toll-like family of receptors recognizes pathogen-associated molecular patterns (PAMPs) from different organisms. TLR4 is the receptor for bacterial lipopolysaccharide (LPS), dsRNA viral mimic poly(I:C) binds to TLR3, and bacterial CpG DNA signals through TLR9. TLR4 signaling is mediated by adaptor molecules Myd88 and TRIF while TLR3 pathway involves only the TRIF adaptor and TLR9 signals solely through Myd88. Methods: To identify genes other than those in TLR pathways that mediate macrophage response to different PAMPs, RAW264.7 cells were stimulated with LPS, poly(I:C), or CpG DNA, and RNA was profiled on microarrays 6 hrs and 24 hrs post-treatment. Gene expression data were analyzed to determine genes, pathways and transcriptional networks that are in common and unique to each of the three TLR stimuli. Potentially novel candidates revealed by this analysis were tested for their role in innate immunity using RNA interference. Results: Many genes are differentially regulated by LPS and poly(I:C) at both 6 hrs and 24 hrs following treatment, while CpG DNA elicits a much less pronounced transcriptional response. By analyzing gene expression data for networks and pathways, we prioritized differentially expressed genes that are in common to all three PAMPs as well as those shared by LPS and poly(I:C). Knockdown by RNA interference of two genes, Plec1 and TPST1, inhibited production of IL-6 in response to LPS in cultured macrophages. Conclusions: We have identified novel innate immunity genes that may be important in macrophage response to LPS, poly(I:C), and CpG DNA stimuli. Our results provide potential biomarkers and therapeutic targets that should be further investigated in mice and human populations. Keywords: time course
2010-10-01 | GSE21548 | GEO
Project description:the proteomics of EspC stimulated RAW264.7 cell lines
2021-09-08 | PXD013666 | Pride
Project description:Nuclear interaction studies by ChIP coupled with mass spectrometry identified the COMPASS/SETD1A complex as interaction partner of the glucocorticoid receptor (GR) in murine bone marrow-derived macrophages (BMDMs). Here, we profiled H3K4me1, H3K4me2 and H3K4me3 in wild-type and Setd1a hypermorphic (Setd1aDel/+) Raw264.7 cells after LPS and Dex+LPS stimulation by spike-in ChIP-Seq.
2020-12-31 | GSE138017 | GEO