Leukotriene D4 induces early genes in Hodgkin lymphoma cells through Cysteinyl leukotriene type I receptor
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE43855 | GEO | 2015/01/01
SECONDARY ACCESSION(S): PRJNA187917
REPOSITORIES: GEO
Similar Datasets
Project description:Human umbilical vein endothelial cells (HUVEC) or the human macrophage cell line, Mono-Mac-6, treated with Leukotriene D4 for 1 hour Keywords = Leukotriene-Transcriptome Keywords = Mono-Mac-6 Keywords = HUVEC Keywords: other
2004-08-20 | GSE1644 | GEO
Project description:Background: Cysteinyl leukotrienes (cysLTs) are important mediators of innate immune responsiveness and chronic inflammatory diseases. CysLTs acting through cysteinyl leukotriene receptors may influence the migration and activity of cells such as eosinophils, monocytes and dendritic cells. Objective: To determine the gene expression signature of human monocytes in response to cysLTs and to elucidate the signaling pathways involved in monocyte activation. Methods: Gene expression was analyzed using oligonucleotide microarrays. Responsiveness to cysLTs was assessed by real-time PCR, calcium flux, kinase activation and chemotaxis assays. Results: Cysteinyl leukotriene type I receptor (CysLTR1) transcript 1 is predominantly expressed in human monocytes and cysLTs signal through CysLTR1 in these cells. Several immediate-early genes, including early growth response (Egr) -2, 3, FosB, activating transcription factor 3 and nuclear receptor subfamily 4 were significantly induced by LTD4. This effect was mediated by CysLTR1 coupled to Gαi/o, activation of phospholipase C, and inositol-1,4,5-triphosphate (IP3) and store operated calcium channels. LTD4 induced p38 MAP kinase phosphorylation, a pathway also involved in the regulation of immediate-early genes expression in monocytes. LTD4 stimulated monocyte chemotactic activity that was fully blocked by a selective CysLTR1 inhibitor MK571 and pertussis toxin, suggesting that CysLTR1 coupled to Gαi/o is a dominant functional pathway in human monocytes. Conclusion: Our data show that cysLTs acting through CysLTR1 can significantly influence the activation and migration of human monocytes and that these effects can be fully inhibited by CysLTR1 antagonists. Clinical implications: Antileukotriene therapies are likely to significantly block the proinflammatory functions of human monocytes. Keywords: monocytes stimulated with LTD4
2007-08-30 | GSE7807 | GEO
Project description:Genomewide gene expression analysis of lymphoid cell lines of Hodgkin, non-Hodgkin and acute leukemia origin Affymetrix U133 Plus 2.0 oligonucleotide arrays were hybridized to determine the gene expression profile of Hodgkin (L428, L1236, KM-H2, HDLM-2, L540, L540Cy), non-Hodgkin (Namalwa, SU-DHL-4) and acute lymphoblastic leukemia (Reh) cell lines; all hybridizations were done in biological duplicates (except L540, L50Cy, SU-DHL-4).
2010-11-17 | E-GEOD-20011 | biostudies-arrayexpress
Project description:Background: Cysteinyl leukotrienes (cysLTs) are important mediators of innate immune responsiveness and chronic inflammatory diseases. CysLTs acting through cysteinyl leukotriene receptors may influence the migration and activity of cells such as eosinophils, monocytes and dendritic cells. Objective: To determine the gene expression signature of human monocytes in response to cysLTs and to elucidate the signaling pathways involved in monocyte activation. Methods: Gene expression was analyzed using oligonucleotide microarrays. Responsiveness to cysLTs was assessed by real-time PCR, calcium flux, kinase activation and chemotaxis assays. Results: Cysteinyl leukotriene type I receptor (CysLTR1) transcript 1 is predominantly expressed in human monocytes and cysLTs signal through CysLTR1 in these cells. Several immediate-early genes, including early growth response (Egr) -2, 3, FosB, activating transcription factor 3 and nuclear receptor subfamily 4 were significantly induced by LTD4. This effect was mediated by CysLTR1 coupled to Gαi/o, activation of phospholipase C, and inositol-1,4,5-triphosphate (IP3) and store operated calcium channels. LTD4 induced p38 MAP kinase phosphorylation, a pathway also involved in the regulation of immediate-early genes expression in monocytes. LTD4 stimulated monocyte chemotactic activity that was fully blocked by a selective CysLTR1 inhibitor MK571 and pertussis toxin, suggesting that CysLTR1 coupled to Gαi/o is a dominant functional pathway in human monocytes. Conclusion: Our data show that cysLTs acting through CysLTR1 can significantly influence the activation and migration of human monocytes and that these effects can be fully inhibited by CysLTR1 antagonists. Clinical implications: Antileukotriene therapies are likely to significantly block the proinflammatory functions of human monocytes. Experiment Overall Design: 4 control sample, 4 LTD4 stimulated samples
2008-06-15 | E-GEOD-7807 | biostudies-arrayexpress
Project description:The aim of the study is to identify miRNA targets in Hodgkin lymphoma cell lines. By immunoprecipitation of wild type Ago2, it is expected to pull down the Ago2 associated gene transcripts. Through microarray analysis, the Ago2 associated gene transcripts identified are expected to be miRNA targets. Keywords: Ribonucleoprotein Immunoprecipitation - Gene Chip (RIP-Chip) RNA isolated from the Ago2 immunoprecipitated (IP) fraction is hybridized against the RNA from total cell lysate (T) fraction. The experiment is performed in two independent Hodgkin lymphoma cell lines, L1236 and L428. In addition, RNA of flow through (FT) fraction of L1236 is hybridized against RNA of total cell lysate (T) fraction of L1236 to demonstrate the specificity/enrichment seen in the IP fraction and not in the FT fraction. All hybridizations is done with a dye swap design.
2010-04-08 | E-GEOD-14409 | biostudies-arrayexpress
Project description:Gene expression analysis was performed from microdissected small and big HRS cells, which were taken from smears of the Hodgkin cell lines L1236 and L428
2017-06-09 | GSE86477 | GEO
Project description:Human umbilical vein endothelial cells (HUVEC) or the human macrophage cell line, Mono-Mac-6, treated with Leukotriene D4 for 1 hour
2008-06-12 | E-GEOD-1644 | biostudies-arrayexpress
Project description:The cysteinyl leukotrienes (cys-LTs) are proinflammatory lipid mediators acting on the type 1 cys-LT receptor (CysLT(1)R) to mediate smooth muscle constriction and vascular permeability. GPR17, a G protein-coupled orphan receptor with homology to the P2Y and cys-LT receptors, failed to mediate calcium flux in response to leukotriene (LT) D(4) with stable transfectants. However, in stable cotransfections of 6xHis-tagged GPR17 with Myc-tagged CysLT(1)R, the robust CysLT(1)R-mediated calcium response to LTD(4) was abolished. The membrane expression of the CysLT(1)R analyzed by FACS with anti-Myc Ab was not reduced by the cotransfection, yet both LTD(4)-elicited ERK phosphorylation and the specific binding of [(3)H]LTD(4) to microsomal membranes were fully inhibited. CysLT(1)R and GPR17 expressed in transfected cells were coimmunoprecipitated and identified by Western blots, and confocal immunofluorescence microscopy revealed that GPR17 and CysLT(1)R colocalize on the cell surface of human peripheral blood monocytes. Lentiviral knockdown of GPR17 in mouse bone marrow-derived macrophages (BMMPhis) increased both the membrane expression of CysLT(1)R protein by FACS analysis and the LTD(4)-elicited calcium flux in a dose-dependent manner as compared with control BMMPhis, indicating a negative regulatory function of GPR17 for CysLT(1)R in a primary cell. In IgE-dependent passive cutaneous anaphylaxis, GPR17-deficient mice showed a marked and significant increase in vascular permeability as compared with WT littermates, and this vascular leak was significantly blocked by pretreatment of the mice with the CysLT(1)R antagonist, MK-571. Taken together, our findings suggest that GPR17 is a ligand-independent, constitutive negative regulator for the CysLT(1)R that suppresses CysLT(1)R-mediated function at the cell membrane.
| S-EPMC2710631 | biostudies-literature
Project description:Background Epigenetic changes are involved in the extinction of the B-cell gene expression program of classical Hodgkin lymphoma. However, little is known regarding epigenetic similarities between classical Hodgkin lymphoma and plasma cell myeloma cells, both of which share an extinction of the gene expression program of mature B-cells. Design and methods Global histone H3 acetylation patterns were determined in cell lines derived from classical Hodgkin lymphoma, plasma cell myeloma and B-cell lymphoma by chromatin immunoprecipitation and subsequent hybridization onto promoter tiling arrays. H3K27 trimethylation was analyzed by chromatin immunoprecipitation and real-time DNA-PCR for selected genes. Epigenetic modifications were compared to gene expression data. Results B-cell characteristic genes were hypoacetylated in classical Hodgkin lymphoma and plasma cell myeloma cell lines, as demonstrated by comparison of their histone H3 acetylation patterns to those of B-cell lines. However, the number of genes jointly hyperacetylated and expressed in classical Hodgkin lymphoma and plasma cell myeloma cell lines, such as IFR4/MUM1 and RYBP, is limited. Moreover, H3K27 trimethylation for selected B-cell characteristic genes revealed that this additional epigenetic silencing is much more prevalent in classical Hodgkin lymphoma as compared to plasma cell myeloma. Conclusion Our epigenetic data support the view that classical Hodgkin lymphoma is characterized by an abortive plasma cell differentiation with a down-regulation of B-cell characteristic genes but without activation of most plasma cell typical genes. Gene expression analysis of Hodgkin lymphoma (cHL) and B-cell lines: Microarray data for three Hodgkin lymphoma cell lines (KM-H2, L1236, L428) and the B-cell line Namalwa that were published previously by our group (GEO accession GSE8388) were analyzed together with newly generated data for the B-cell lines SU-DHL4 and SU-DHL6. For all cell lines, RNA was isolated according to standard protocols (Qiagen, Hilden, Germany) and used for Affymetrix GeneChip hybridization (HG-U133A). Microarrays were normalized using RMA, and differential expression was calculated using moderated t-test. The gene expression profiles of the cell lines were generated in duplicates.
2011-05-05 | E-GEOD-21251 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE25986: Gene expression profiling of cell lines derived from classical Hodgkin lymphoma GSE25987: Gene expression profiling of Hodgkin lymphoma cell line KMH2: Comparison of CIITA-BX648577 knockdown cultures with non-silencing controls GSE25989: Copy number analysis of Hodgkin lymphoma cell lines KM-H2 and L-428 Refer to individual Series *** This submission represents the microarray gene expression and microarray copy number components of the study
2010-12-11 | E-GEOD-25990 | biostudies-arrayexpress