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Dectin-1-mediated signaling leads to characteristic gene expressions in rat mast cells

ABSTRACT: Rat mast cell line RBL-2H3 was analyzed to investigate the molecular mechanism of Dectin-1-mediated activation and responses of mast cells. Dectin-1-mediated signaling stimulated characteristic gene expression, such as MCP-1, IL-4, IL-13, TNF-αand Nfkbiz. RBL-2H3 cell line stably expressing Dectin-1 was established. Non-stimulated cells (control) compared to Dectin-1-stimulated (Curdlan) cells in order to comfirm Dectin-1-mediated signaling-inducible genes. Dectin-1-stimulated cells compared to Syk inhibitor R406-pretreated cells in order to examine the importance of Syk for Dectin-1-mediated gene up-regulations.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Yukihiro Kimura

PROVIDER: E-GEOD-56246 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Dectin-1-mediated signaling leads to characteristic gene expressions in rat mast cells

Project description:Rat mast cell line RBL-2H3 was analyzed to investigate the molecular mechanism of Dectin-1-mediated activation and responses of mast cells. Dectin-1-mediated signaling stimulated characteristic gene expression, such as MCP-1, IL-4, IL-13, TNF-αand Nfkbiz.

2014-03-27 | GSE56246 | GEO

Gene expression profiling of five diffuse large B-cell lymphoma (DLBCL) cell lines, DHL4, DHL6, LY7, HBL1 and U2932, treated with the SYK inhibitor, R406

2013-08-31 | GSE43510 | GEO

Gene expression profiling of two diffuse large B-cell lymphoma (DLBCL) cell lines, DHL4 and DHL6, treated with the SYK inhibitor, R406

2013-12-31 | GSE34176 | GEO

Gene expression profiling of five diffuse large B-cell lymphoma (DLBCL) cell lines, DHL4, DHL6, LY7, HBL1 and U2932, treated with the SYK inhibitor, R406

Project description:The five DLBCL cell lines were treated with R406 to assess the signature of SYK inhibition. In previous studies, R406 decreased the proliferation and induced apoptosis of these surface Ig+ cell lines. In the previous studies, R406 inhibited the autophosphorylation of SYK 525/526 and SYK-dependent phosphorylation of BCR signaling components such as BLNK. RNA samples from five DLBCL cell lines treated with R406 or vehicle (DMSO) alone for 0, 6, or 24 hours were profiled in triplicate on Affymetrix HT_HG-U133plust2 chips.

2013-08-31 | E-GEOD-43510 | biostudies-arrayexpress

Gene expression profiling of two diffuse large B-cell lymphoma (DLBCL) cell lines, DHL4 and DHL6, treated with the SYK inhibitor, R406

Project description:The two DLBCL cell lines were treated with R406 to assess the signature of SYK inhibition. In previous studies, R406 decreased the proliferation and induced apoptosis of these surface Ig+ cell lines. In the previous studies, R406 inhibited the autophosphorylation of SYK 525/526 and SYK-dependent phosphorylation of BCR signaling components such as BLNK. RNA samples from two DLBCL cell lines, DHL4 and DHL6, treated with R406 or vehicle (DMSO) alone for 0, 2, 6, 24 or 48 hours were profiled in triplicate on Affymetrix HT_HG-U133A chips.

2013-12-31 | E-GEOD-34176 | biostudies-arrayexpress

Transcription profiling of mouse MyD88-deficient bone marrow-derived macrophages treated with Zymosan

Project description:Innate immune pattern recognition receptors play critical roles in pathogen detection and initiation of antimicrobial responses. We and others have previously demonstrated the importance of the beta-glucan receptor Dectin-1 in the recognition of pathogenic fungi by macrophages and dendritic cells, and have elucidated some of the mechanisms by which Dectin-1 signals to coordinate the antifungal response. While Dectin-1 signals alone are sufficient to trigger phagocytosis and Src-Syk-mediated induction of antimicrobial reactive oxygen species, collaboration with Toll-like receptor (TLR)2 signaling enhances NF-kB activation and regulates cytokine production. In this study we demonstrate that Dectin-1 signaling can also directly modulate gene expression via activation of nuclear transcription of activated T cells (NFAT) transcription factors. Dectin-1 ligation by zymosan particles or live Candida albicans yeast triggers NFAT activation in macrophages and dendritic cells. Dectin-1-triggered NFAT activation plays a role in the induction of Egr2 and Egr3 transcription factors, and cyclooxygenase 2 (Cox-2). Furthermore, we show that NFAT activation regulates IL-2, IL-10 and IL-12 p70 production by zymosan-stimulated dendritic cells. These data establish NFAT activation in myeloid cells as a novel mechanism of regulation of the innate antimicrobial response. Experiment Overall Design: Bone marrow-derived macrophages deficient in MyD88 were stimulated with zymosan, and total RNA was extracted 120 minutes after stimulation for comparison to macrophages grown under the same conditions, but not stimulated.

2008-06-14 | E-GEOD-6376 | biostudies-arrayexpress

R406-Inhibition of Syk-Cn-NFAT Signaling Axis Promotes Chemical Reprogramming via Metabolic Rewiring and H2S Production

Project description:Small molecules not only are convenient and useful for controlling cell fates, but also can provide better understanding of the molecular mechanisms of cell-fate transitions. Here, we identified that spleen tyrosine kinase (Syk) inhibitor R406 could significantly promote the early stage of mouse chemical reprogramming. Furthermore, R406 alleviated the Syk-calcineurin (Cn)-nuclear factor of activated T cells (NFAT) signaling cascade-mediated suppression of glycine, serine and threonine metabolic genes transcriptionally, which is previously unrecognized. In turn, R406 upregulated metabolites of glycine, serine and threonine metabolism and downstream transsulfuration cysteine biosynthesis pathway and cysteine metabolism. Subsequently, increased cellular hydrogen sulfide (H2S) after R406 treatment downregulated oxidative phosphorylation (OXPHOS) and reactive oxygen species (ROS), modulated redox homeostasis, and significantly enhanced chemical reprogramming. In sum, our studies have not only improved the chemical reprogramming technique, but also identified interesting molecular mechanisms of chemical-induced pluripotent reprogramming, which hold great potentials in regenerative medicine.

2021-03-14 | GSE154687 | GEO

BLNK negatively regulates C-type lectin receptor-mediated antifungal immunity through inhibiting macrophage migration

Project description:B cell linker protein (BLNK) is a pivotal adaptor protein that interfaces the B cell receptor (BCR)-associated spleen tyrosine kinase (Syk) to regulate B cell function and development. However, it is still not well understood whether BLNK is involved in Syk-coupled C-type lectin receptor (CLR) signaling in myeloid cells, particularly in the context of antifungal immunity. Here, we show that stimulation with fungi-derived β-glucans or α-mannans induced the phosphorylation of BLNK in macrophages, which was significantly impaired due to the deficiency of CLRs including Dectin-1 and Dectin-2, as well as their downstream mediators Syk and Fc-receptor gamma-chain (FcRγ). Furthermore, BLNK is induced to be interacted with casitas B-lineage lymphoma (c-Cbl), which is completely dependent on the engagement of Dectin-1 and Dectin-2. Notably, BLNK deficiency facilitates CLR-mediated recruitment of c-Cbl/phosphatidylinositol 3-kinase (PI3K) complex to F-actin cytoskeleton, thereby promoting macrophage migration. Consequently, mice with monocyte-specific deficiency of BLNK are highly resistant to the infection with Candida albicans, a major human fungal pathogen, through increasing the infiltration of Ly6C+macrophages into kidneys. Together, our data indicate that BLNK functions downstream of Syk-coupled CLRs to negatively regulate antifungal immunity against C. albicans infection. These findings unravel a previously unidentified role of BLNK that negatively regulates macrophage migration through inhibiting CLR-mediated recruitment of c-Cbl/PI3K complex to the cytoskeleton.

2023-11-07 | GSE246891 | GEO

Zymosan stimulation of MyD88-deficient bone marrow-derived macrophages

2007-01-30 | GSE6376 | GEO

in vitro ubiquitination by E3 ligase Cbl-b

Project description:Fungal infections claim an estimated 1.5 million lives every year. Mechanisms that protect from fungal infections are still elusive. Recognition of fungal pathogens relies on C-type lectin receptors (CLR) and their downstream signaling kinase SYK. Here we report that the E3-ubiquitin-ligase CBL-B controls proximal C-type lectin receptor signaling in macrophages and dendritic cells. We show that CBL-B associates with SYK and ubiquitinates SYK, Dectin-1, and Dectin-2 upon fungal recognition. Functionally, CBL-B deficiency results in increased inflammasome activation, enhanced reactive oxygen species production, and increased fungal killing. Genetic deletion of Cblb protects mice from morbidity caused by cutaneous infection and markedly improves survival upon a lethal systemic infection with Candida albicans. Based on these findings, we engineered a cell-permeable CBL-B inhibitory peptide that protects mice from lethal C. albicans infections. We thus describe a key role for Cblb in the regulation of innate anti-fungal immunity and establish a novel paradigm for the treatment of fungal sepsis.

2016-06-17 | PXD004256 | Pride

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