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Differential expression of Hdc-GFP+/hiCD11b+Gr1lo vs Hdc-GFP+/hiCD11b+Gr1hi myeloid cells from mouse bone marrow

ABSTRACT: 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.

OTHER RELATED OMICS DATASETS IN: PRJNA316854

ORGANISM(S): Mus musculus

PROVIDER: GSE80143 | GEO | 2019/04/01

REPOSITORIES: GEO

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Differential expression of Hdc-GFP+/hiCD11b+Gr1+ vs Hdc-GFP-/loCD11b+Gr1+ myeloid cells from mouse bone marrow

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

Differential expression of Hdc-GFP+/hi HSC VS Hdc-GFP-/lo hematopoetic stem cells (HSCs) from bone marrow.

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

The Hdc GC box is critical for Hdc gene transcription and histamine-mediated anaphylaxis [ATAC-Seq]

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

The Hdc GC box is critical for Hdc gene transcription and histamine-mediated anaphylaxis [CUT&Tag]

2023-02-23 | GSE223386 | GEO

HDC/histamine signaling axis drives macrophage reprogramming to promote angiogenesis in the hindlimb ischemia mice

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

Differentially expressed genes of CD11b+Gr-1+ myeloid cells

2010-12-15 | GSE23502 | GEO

Mus musculus

Project description:Differential expression of Hdc-GFP+/hiCD11b+Gr1+ vs Hdc-GFP-/loCD11b+Gr1+ myeloid cells from mouse bone marrow

| PRJNA316854 | ENA

Differentially expressed genes of CD11b+Gr-1+ myeloid cells

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

White matter abnormalities in the Hdc knockout mouse, a model of tic and OCD pathophysiology

Project description:An inactivating mutation in the histidine decarboxylase gene (Hdc) has been identified as a rare but high-penetrance genetic cause of Tourette syndrome (TS). TS is a neurodevelopmental syndrome characterized by recurrent motor and vocal tics; it is accompanied by structural and functional abnormalities in the cortico-basal ganglia circuitry. Hdc, which is expressed both in the posterior hypothalamus and peripherally, encodes an enzyme required for the biosynthesis of histamine. Hdc knockout mice (Hdc-KO) recapitulate this mutation and exhibit behavioral and neurochemical abnormalities that parallel those seen in patients with TS. Exploratory RNA-Seq analysis revealed, unexpectedly, that genes associated with oligodendrocytes and with myelin production are upregulated in the dorsal striatum of these mice. This was confirmed by qPCR and immunoblotting. These results suggest an abnormality in myelination in the striatum. To test this in an intact brain, we performed whole-brain ex vivo diffusion tensor imaging (DTI), which revealed reduced fractional anisotropy (FA) in the mid-dorsal striatum. While the DTI literature in individuals with TS is sparse, these results are consistent with findings of disrupted descending cortical projections in patients with tics. The Hdc-KO model may represent a powerful system in which to examine the developmental mechanisms underlying this abnormality.

2023-01-04 | GSE161252 | GEO

Gene expression data from 1 year old Hdc+/+ and Hdc-/- stomach.

Project description:Histamine defeciency result to hypertrophic gastropathy in the stomach. We use gene array to distover the major cause of stomach lesion in Hdc-/-. Tesult shows that chronic inflammation and dysregulation of macrophage functions are the major trigger for hypertrophic gastropathy in Hdc--/- stomach.

2022-09-14 | GSE213293 | GEO

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