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Expression data from HMC-1 mast cells

ABSTRACT: We demonstrate that the G protein Gi3 is the cellular target of the adenosine A3 receptor (A3R). By using a cell permeable peptide comprising the C-terminal end of Gαi3 fused to an importation sequence (ALL1) as a selective inhibitor of Gi3 signaling, we show that by coupling to Gi3, the A3R stimulates multiple signaling pathways in human mast cells, leading to upregulation of cytokines, chemokines and growth factors.Following contact with activated T cell membranes, endogenous adenosine binds to and activates the A3R, resulting in Gi3-mediated signaling. Specifically, the majority of ERK1/2 signaling initiated by contact with activated T cell membranes, is mediated by Gi3, giving rise to ALL1-inhibitable cellular responses. These results unveil the physiological GPCR that couples to Gi3 and establish the important role played by this G-protein in inflammatory conditions that involve adenosine-activated mast cells. We used microarrays to detail the effect of ALL1 on gene expression of HMC-1 cells activated directly by the A3 receptor, or by contact with activated T cell membranes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE19888 | GEO | 2010/03/31

SECONDARY ACCESSION(S): PRJNA122029

REPOSITORIES: GEO

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Expression data from HMC-1 mast cells

Project description:We demonstrate that the G protein Gi3 is the cellular target of the adenosine A3 receptor (A3R). By using a cell permeable peptide comprising the C-terminal end of GÎ±i3 fused to an importation sequence (ALL1) as a selective inhibitor of Gi3 signaling, we show that by coupling to Gi3, the A3R stimulates multiple signaling pathways in human mast cells, leading to upregulation of cytokines, chemokines and growth factors.Following contact with activated T cell membranes, endogenous adenosine binds to and activates the A3R, resulting in Gi3-mediated signaling. Specifically, the majority of ERK1/2 signaling initiated by contact with activated T cell membranes, is mediated by Gi3, giving rise to ALL1-inhibitable cellular responses. These results unveil the physiological GPCR that couples to Gi3 and establish the important role played by this G-protein in inflammatory conditions that involve adenosine-activated mast cells. We used microarrays to detail the effect of ALL1 on gene expression of HMC-1 cells activated directly by the A3 receptor, or by contact with activated T cell membranes. The experiment consisted of 6 treatments in duplicates, a total of 12 samples. The cells were activated via two different activation pathways (A3 and T membranes), with or without pretreatment with the drug ALL1.

2010-04-12 | E-GEOD-19888 | biostudies-arrayexpress

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Project description:Humans mast cell line-1 (HMC-1) cultured with or without hypoxia for indicated time period were analysed

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Gene expression data from NECA (5/-N-ethylcarboxamidoadenosine) treated murine pituitary folliculostellate cells(TtT/GF)

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A novel Cpa3-Cre; miR-9∆fl/∆fl mouse reveals a functional role for miR-9 in promoting a mast cell invasive phenotype via upregulation of CMA1

Project description:The purpose of this study was to investigate the biologic consequences of miR-9 overexpression in normal mast cells and interrogate the mechanisms by which mir-9 enhances invasion. We generated a transgenic mouse line carrying a floxed-STOP-miR-9 transgene (miR-9∆fl/∆fl) and crossed it with Cpa3-Cre transgenic mice in which Cre recombinase expression is restricted largely to mast cells and basophils, by the carboxypeptidase A3 (Cpa3) promoter. RNA-seq revealed a unique transcriptional profile associated with miR-9 overexpression in BMCMCs, notably up-regulation of mast cell-restricted proteases CMA1 and MCP6 involved in extracellular matrix remodeling. Targeting of the transcriptional corepressor SIN3A by miR-9 enhanced CMA1 expression, indicating a novel regulatory pathway through which miR-9 upregulates CMA1 expression, thereby promoting an invasive phenotype. These data support a role for miR-9 in mast cell invasive properties and provide a mechanism through which dysregulation of miR-9 in mast cells may contribute to pathologic conditions involving mast cell-mediated tissue remodeling.

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A glycoanalysis of WEHI 231 B cell line to determine if there is a different profile of carbohydrates following apoptosis, especially if there is an exposure of fucose residues

Project description:We have determined that there is a carbohydrate change on CD44 on leukocytes during apoptosis. This change is important for phagocytosis of the apoptotic cells and is inhibitable by fucoidin but not mannan or monosaccharides. In addition, this occurs without new protein synthesis. We want to immunoprecipitate CD44 from apoptotic and control cells and determine whether there is a different profile of carbohydrates, especially exposure of fucose residues. We have used a lectin to isolate a protein consistent with the molecular weights of CD44. We would also like to do a profile of the apoptotic versus control membranes from the B cells as a comparison. RNA preparations were sent to the Microarray Core (E). The RNA was amplified, labeled, and hybridized to the GLYCOv3 microarrays. Data was provided to Dr. Mills' laboratory for analysis.

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Gene expression data from NECA (5/-N-ethylcarboxamidoadenosine) treated murine pituitary folliculostellate cells(TtT/GF)

Project description:Folliculostellate cells constitute as much as 10% of the cells within the anterior pituitary gland; they however do not secrete any of the classical hormones but do express cytokines and growth factors. The endogenous nucleoside adenosine can be either pro- or anti-inflammatory depending on receptor expression and the activation of one or more receptors A1, A2a, A2b and A3. Adenosine stimulates the secretion of immune molecules from folliculostellate; these cells appear to mediate communication between the endocrine and immune systems. Replicate (x3) cultures of TtT/GF cells were treated with 10µM NECA (5/-N-ethylcarboxamidoadenosine) for 30 and 120 minutes. RNA was extracted, cRNA prepared and hybridized to murine MG_U74A v2 GeneChip (Affymetrix), changes in expression were compared with untreated controls.

2009-04-08 | E-GEOD-15564 | biostudies-arrayexpress

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