Differentially expressed genes of CD11b+Gr-1+ myeloid cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE23502 | GEO | 2010/12/15
SECONDARY ACCESSION(S): PRJNA131071
REPOSITORIES: GEO
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Project description:Differentially expressed genes of CD11b+Gr-1+ immature myeloid cells (IMCs) in the bone marrow and colonic tumor setting of histidine decarboxylase (HDC)-KO mice were examined by microarray (Affymetrix Mouse 430.2 array). Myeloid differentiation-related candidate genes were sought to be isolated and functionally studied. Total RNA of HDC-expressing CD11b+Gr-1+ IMCs of bone marrow were extracted from HDC-EGFP and HDC-EGFP/HDC-KO mice (3 mice in each group). CD11b+Gr-1+ myeloid-derived suppressor cells (MDSCs) of colon tumor were sorted from 10-12 colon tumors of WT and HDC-KO mice (5 mice in each group), and pooled to extract total RNA for microarray studies. Two technical replicates for each of the four groups. Four sets of comparisons were performed to screen for upregulated or downregulated genes in the HDC-KO CD11b+Gr-1+ IMCs or MDSCs (experiment group) compared to the WT group: (1) HDC-expressing CD11b+Gr-1+ IMCs of bone marrow of HDC KO mice compared to bone marrow IMCs of WT mice; (2) CD11b+Gr-1+ MDSCs in tumors of HDC-KO mice compared to WT mice; (3) CD11b+Gr-1+ MDSCs of WT colon tumors compared to IMCs in the WT bone marrow; and (4) CD11b+Gr-1+ MDSCs of colon tumors of HDC-KO mice compared to IMCs in the bone marrow of HDC-KO mice.
2010-12-15 | E-GEOD-23502 | biostudies-arrayexpress
Project description:Bone marrow Hdc-GFP+/hiCD11b+Gr1lo vs Hdc-GFP+/hiCD11b+Gr1hi myeloid cells were isolated from bones from histidine decarboxylase (Hdc) green fluorescent protein (Hdc-GFP) mice. Hdc-GFP+/hiCD11b+Gr1hi cells and Hdc-GFP+/hiCD11b+Gr1/lo cells were sorted by combinations of GFP and myeloid cell surface markers CD11b and Gr1 and their differential mRNA expression compared with Affymetrix microarrays.
2019-04-01 | GSE80143 | GEO
Project description:Bone marrow Hdc-GFP+/hi and Hdc-GFP-/loCD11b+Gr1+ cells were isolated from bones from histidine decarboxylase (Hdc) green fluorescent protein (Hdc-GFP) mice Hdc-GFP+/hiCD11b+Gr1+ cells and Hdc-GFP-/loCD11b+Gr1+ cells were sorted by combinations of GFP and myeloid cell surface markers CD11b and Gr1 and their differential mRNA expression compared with Affymetrix microarrays.
2017-08-22 | GSE79728 | GEO
Project description:We extracted RNA of sorted splenic CD11b+Gr-1+ cells and performed microarray analyses. Total RNA was isolated using the manufacturer’s recommended protocol for RNeasy (Qiagen, Valencia, CA). Isolated RNA was quantified, and quality was assessed using an Agilent A 2100 BioAnalyzer with the RNA NanoChip (Agilent, Andover, MA). We used 2μg of total RNA to make single-stranded antisense cDNA with the NuGEN Technologies (San Carlo, CA) Ovation Biotin System in accordance with the manufacturer’s directions. Labeled targets were hybridized to Affymetrix (Santa Clara, CA) MOE430 2.0 GeneChip microarrays for 16h at 45°C. The arrays were washed and scanned according to Affymetrix standard protocols. We used microarrays to detail the global gene expression of CD11b+Gr-1+ cells from the control mice and the clarithromycin-treated mice, and identified distinct classes of up-regulated genes during this process.
2016-05-09 | GSE81241 | GEO
Project description:Histamine is a critical mediator of anaphylaxis, a neurotransmitter, and a regulator of gastric acid secretion. Histidine decarboxylase is a rate-limiting enzyme for histamine synthesis. However, in vivo regulation of Hdc, the gene that encodes histidine decarboxylase is poorly understood. We sought to investigate how enhancers regulate Hdc gene transcription and histamine synthesis in resting conditions and in a mouse model of anaphylaxis. H3K27 acetylation histone modification and chromatin accessibility were used to identify candidate enhancers; The enhancer activity of candidate enhancers was measured in a reporter gene assay; and the function enhancers were validated using CRISPR deletion. Deletion of the GC box, which binds to zinc finger transcription factors, in the proximal Hdc enhancer, reduced Hdc gene transcription and histamine synthesis in the mouse and human mast cell lines. Mast cells, basophils, brain cells, and stomach cells from GC box-deficient mice transcribed the Hdc gene much less than similar cells from wild-type mice and Hdc GC box-deficient mice failed to develop anaphylaxis. Our results demonstrate that the HDC GC box within the proximal enhancer in the mouse and human HDC gene is essential for Hdc gene transcription, histamine synthesis, and histamine-mediated anaphylaxis in vitro and in vivo.
2023-02-23 | GSE223386 | GEO
Project description:Histamine is a critical mediator of anaphylaxis, a neurotransmitter, and a regulator of gastric acid secretion. Histidine decarboxylase is a rate-limiting enzyme for histamine synthesis. However, in vivo regulation of Hdc, the gene that encodes histidine decarboxylase is poorly understood. We sought to investigate how enhancers regulate Hdc gene transcription and histamine synthesis in resting conditions and in a mouse model of anaphylaxis. H3K27 acetylation histone modification and chromatin accessibility were used to identify candidate enhancers; The enhancer activity of candidate enhancers was measured in a reporter gene assay; and the function enhancers were validated using CRISPR deletion. Deletion of the GC box, which binds to zinc finger transcription factors, in the proximal Hdc enhancer, reduced Hdc gene transcription and histamine synthesis in the mouse and human mast cell lines. Mast cells, basophils, brain cells, and stomach cells from GC box-deficient mice transcribed the Hdc gene much less than similar cells from wild-type mice and Hdc GC box-deficient mice failed to develop anaphylaxis. Our results demonstrate that the HDC GC box within the proximal enhancer in the mouse and human HDC gene is essential for Hdc gene transcription, histamine synthesis, and histamine-mediated anaphylaxis in vitro and in vivo.
2023-02-23 | GSE223387 | GEO
Project description:Bone marrow Hdc-GFPhi and Hdc-GFPlo HSPC (SLAM-LSK, Lin-c-kit+Sca-1+CD150+CD48-) HSCs were isolated from mouse femur and tibia from histidine decarboxylase (Hdc) green fluorescent protein (Hdc-GFP) mice. Hdc-GFPhi HSC and Hdc-GFPlo HSC cells were sorted by combinations of GFP and the cell surface markers of HSC. total RNA was isolated from sorted 2,500 HSPCs using ARCTURUS PicoPure RNA isolation kit (Life Technologies). cDNA was amplified and libraries were constructed by using SMARTer Ultra Low Input RNA kit (Clontech Laboratories) and Nextera XT DNA Library Preparation kit (Illumina) according to manufacturer’s instructions respectively. Sequencing was performed on the Illumina HiSeq2000 platform.
2019-11-20 | GSE90787 | GEO
Project description:The gene expression of murine splenic myeloid derived suppressor cells treated with Tff2 is characterized. The motivation of the study originates in the fact that Gr1+Cd11b+ myeloid-derived suppressor cells (MDSCs), which resemble immature myeloid cells (IMCs), expand during cancer in response to inflammatory cytokines and accumulate in the spleen. MDSCs promote neoplastic progression through their suppression of anti-tumourigenic cytotoxic T-cells. MDSCs are also rapidly expanded following acute insults, but in cancer as opposed to acute inflammation, MDSCs persist. It is now recognized that a vagally-mediated, anti-inflammatory reflex arc promoting acetylcholine secretion by Cd4+ (Cd44hiSelllo) T cells, is necessary for a return to homeostasis after an acute insult. Failure of this restorative neural circuit might contribute to unabated procarcinogenic inflammation, with the chronic expansion of MDSCs driving carcinogenesis. Trefoil factor 2 (Tff2) is a secreted anti-inflammatory peptide produced by both epithelial cells and a small subset of splenic T cell. In this study, we show that splenic Tff2 is induced in vagally-modulated memory T cells to suppress the expansion of MDSCs in response to chemical and carcinogenic injury. Deletion of Tff2 interrupts this anti-inflammatory neural arc and leads to expanded MDSCs and a dramatically increased incidence of colorectal cancer. Tff2 directly suppresses proliferation of myeloid progenitors, in a large part through upregulation of cell-bound Apolipoprotein E (ApoE), which has previously been shown to suppress proliferation of haematopoietic stem and progenitor cells. The predisposition to inflammation-associated cancer can be rescued through transgenic overexpression of splenic Tff2, adenoviral transfer of Tff2 expression or transplantation of Tff2-expressing haematopoietic cells. Thus, Tff2 production in memory T cells, is regulated by the vagus nerve, plays a central role in arresting procarcinogenic MDSC proliferation, and offers a novel approach to the prevention and treatment. A. Gr1+Cd11b+ splenic cells from Tff2-/- mice treated with Csf2 (n=4). B. Gr1+Cd11b+ splenic cells from Tff2-/- mice treated with Tff2 and Csf2 (n=4).
2016-05-30 | E-GEOD-47596 | biostudies-arrayexpress
Project description:Gr-1+ myeloid cells are recruited in prostate conditioanal Pten null tumours (Ptenpc-/-). To identify the secreted factors that may be released by Gr-1+ cells and epithelial cells in the tumour microenvironment, we compared, by gene expression analysis, the cytokine profile of Gr-1+ myeloid cells sorted from Ptenpc-/- tumours with the profile of immune cell-depleted Ptenpc-/- epithelial cells. qRT-PCR validation for IL-10, IL1rn, IL-1α, IL-6, VEGF, TNFα, CXCL1, CCL2 and CXCL12 was also performed. Pten pc-/- 8 weeks old mice were sacrificed and whole prostates were isolated and processed to single cell suspension. mRNA from sorted Gr-1+ myeloid cells and epithelial cells was used for gene expression analysis. Cells sorted from 3 mice/each experiment were pulled together. 2 independent experiments were performed.
2014-06-13 | E-GEOD-58413 | biostudies-arrayexpress
Project description:Histamine is catalyzed by histidine decarboxylase (HDC), which plays important roles in many physiological and pathological processes, but its role in angiogenesis has not been thoroughly clarified. Here we report that HDC is highly expressed in Ly6C+macrophages, rather than in endothelial cells using Hdc-GFP transgenic mice with hindlimb ischemia (HLI) mouse model. Given the whole-process promoting effect of macrophages on angiogenesis, a cluster of HDC+CXCR2+ macrophages have been identified by single-cell sequencing technology in ischemic tissue. The inactivation of HDC leads to a lack of histamine and pro-angiogenic factor production in macrophages, inducing a harsh inflammatory microenvironment that is not conducive to the interaction between macrophages and endothelial cells. Moreover, HA-DA@histamine hydrogel has been designed and demonstrated to safely treat ischemic injury by modulating inflammation and angiogenesis. These data highlight the critical roles of HDC/histamine signaling in macrophage differentiation, angiogenesis, and muscle regeneration in the early stage of HLI.
2024-08-02 | GSE273730 | GEO