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Chromatin accessibility analysis of adipose progenitors (AP).

ABSTRACT: We hypothesized that core transcriptional regulatory circuitries analysis could be used in conjunction with gene expression profiling data to nominate specific TFs for additional functional studies of AP cell state. To accomplish this analysis, we utilized the assay of transposase-accessible chromatin coupled to massively parallel sequencing (ATAC-seq) to identify putative enhancers in APs. The AP preparation involved adipose tissue digestion, and negative selection of the stromal vascular fraction (depletion of CD31+ endothelial cells and Lineage positive cells).

ORGANISM(S): Mus musculus

PROVIDER: GSE118856 | GEO | 2018/08/22

REPOSITORIES: GEO

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Gene expression profiling of adipocyte precursor cells (AP) nonwounded and day 5 wound beds

Project description:APs were isolated from naïve skin and day 5wounds from dorsal skin wound beds of 7-9 weeks old using FACS. This experiment describes changes in AP gene expression associated with injury and subsequent tissue repair.

2018-11-06 | GSE105788 | GEO

Transcriptomic analysis of wild type and Nr4a1-/- adipose progenitors.

Project description:The project aims to identify differentially expressed genes in adipose progenitors that were freshly isolated from wild-type or Nr4a1-/- mice. The AP preparation involved adipose tissue digestion, and negative selection of the stromal vascular fraction (depletion of CD31+ endothelial cells and Lineage positive cells.

2018-08-22 | GSE118879 | GEO

Single-cell sequencing of pancreatic tissues of mice with acute pancreatitis under the background of normal diet and high-fat diet was compared

Project description:Background: Acute pancreatitis (AP) is a common severe digestive disorder, with severity linked to high-fat diets (HFD). HFD may exacerbate AP by promoting inflammation and altering gut microbiota. Astragalus polysaccharides (APS) possess anti-inflammatory properties, but it is unclear if APS supplementation can mitigate HFD's detrimental effects on AP by modulating gut microbiota. This study investigates the mechanisms by which APS improves HFD-induced AP exacerbation. In this study, C57BL/6 mice were fed HFD or a standard diet, with or without APS, for 12 weeks. AP was induced via intraperitoneal caerulein injection. Analyses included ELISA, Western blotting, histology, immunohistochemistry, immunofluorescence, single-cell RNA sequencing (scRNA-seq), 16S rRNA sequencing of gut microbiota, and short-chain fatty acid (SCFA) analysis to evaluate inflammation and cellular changes. Results: HFD significantly increased AP severity, indicated by elevated serum enzyme and pro-inflammatory cytokine levels, along with extensive pancreatic damage. Single-cell RNA sequencing (scRNA-seq) showed a notable rise in ICAM1+ neutrophils and activation of the NF-κB/necroptosis pathway in HAP mice. APS alleviated these effects by decreasing ICAM1+ neutrophil infiltration, downregulating the NF-κB pathway, and reducing necroptosis. Moreover, APS restored gut microbiota balance, significantly boosting Lactobacillus reuteri (L. reuteri) abundance and propionate (PA) levels. Treatments with L. reuteri and PA independently mitigated HFD-induced AP severity, indicating that APS's protective effects are microbiota-dependent. Conclusion: APS improves HFD-induced gut dysbiosis and intestinal barrier dysfunction by enriching L. reuteri and PA, effectively reducing AP exacerbation. Our findings highlight the gut-pancreas axis as a promising target for addressing AP severity.

2024-10-22 | GSE279876 | GEO

Cell cycle-independent temporal identity transitions in cortical progenitor cells as revealed by single cell transcriptome analysis

Project description:During cerebral development, a variety of neurons are sequentially generated by self-renewing progenitor cells, apical progenitors (APs). A temporal change in AP identity is thought to produce a diversity of progeny neurons, while underlying mechanisms are largely unknown. Here we performed single cell genome-wide transcriptome profiling of APs at different neurogenic stages, and identified a set of genes that are temporally expressed in APs in a manner independent of differentiation state. Surprisingly, the temporal pattern of such AP gene expression was not affected by arresting cell cycling. Consistently, a transient cell cycle arrest of APs in vivo did not prevent descendant neurons to acquire their correct laminar fates. in vitro cell culture of APs revealed that transitions in AP gene expression involved in both cell-autonomous and non-autonomous mechanisms. These results suggest that timers controlling AP temporal identity run independently of cell cycle progression and Notch activation mode.　

2016-04-07 | GSE55981 | GEO

3-AP and Gemcitabine in Treating Patients With Advanced Solid Tumors or Lymphoma

Project description:This phase I trial is studying the best dose of 3-AP and the side effects of giving 3-AP together with gemcitabine in treating patients with advanced solid tumors or lymphoma. Drugs used in chemotherapy, such as 3-AP and gemcitabine (GEM), work in different ways to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. 3-AP may help gemcitabine kill more cancer cells by making the cells more sensitive to the drug. 3-AP may also stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

| 2026481 | ecrin-mdr-crc

Estrogen regulation and physiopathologic significance of alternative promoters in breast cancer

Project description:Alternative promoters (APs) occur in >30% protein-coding genes and contribute to proteome diversity. However, large-scale analyses of AP regulation are lacking, and little is known about their potential physiopathologic significance. To better understand the transcriptomic impact of estrogens, which play a major role in breast cancer, we analyzed gene and AP regulation by estradiol in MCF7 cells using pan-genomic exon arrays. We thereby identified novel estrogen-regulated genes, and determined the regulation of AP-encoded transcripts in 150 regulated genes. In <30% cases, APs were regulated in a similar manner by estradiol, while in >70% cases, they were regulated differentially. The patterns of AP regulation correlated with the patterns of estrogen receptor (ERα) and CCCTC-binding factor (CTCF) binding sites at regulated gene loci. Interestingly, among genes with differentially regulated APs, we identified cases where estradiol regulated APs in an opposite manner, sometimes without affecting global gene expression levels. This promoter switch was mediated by the DDX5/DDX17 family of ERα coregulators. Finally, genes with differentially regulated promoters were preferentially involved in specific processes (e.g., cell structure and motility, and cell cycle). We show in particular that isoforms encoded by the NET1 gene APs, which are inversely regulated by estradiol, play distinct roles in cell adhesion and cell cycle regulation, and that their expression is differentially associated with prognosis in ER+ breast cancer. Altogether, this study identifies the patterns of AP regulation in estrogen-regulated genes, demonstrates the contribution of AP-encoded isoforms to the estradiol-regulated transcriptome, as well as their physiopathologic significance in breast cancer.

2010-02-17 | GSE20342 | GEO

Role of AP-2a/AP-2b transcription factors in the adult epidermis.

Project description:To investigate the effects of inactivation of the transcription factors AP-2a and/or AP-2b in the adult mouse skin.

2023-12-20 | GSE248372 | GEO

Generation of a new mouse model of glaucoma characterized by reduced expression of the AP-2 and AP-2

Project description:This study reports on the generation of a transgenic mouse which is characterized by early-onset angle-closure glaucoma. The phenotype is due to the transgene insertion site which is proximal to the genes encoding AP-2 and AP-2, two proteins present in the retina and corneal epithelium. This leads to a reduction in AP-2 levels, which is likely to are responsible for the glaucomatous phenotype. Here we provide paired-end raw DNA-Seq reads of the transgenic mouse genome.

2017-03-10 | E-MTAB-5502 | biostudies-arrayexpress

Targeting genes of AP-2d in the mouse midbrain

Project description:Identification of AP-2d target genes in the midbrain of E15 mouse embryos RNA from a pool of 15 E15 mouse midbrains from control and AP-2d knockout embryos

2011-07-31 | E-GEOD-27296 | biostudies-arrayexpress

Genome-wide maps of apurinic sites (AP-sites) and 8-oxoG derived secondary AP-sites

Project description:We developed a novel method, AP-seq, capable of mapping apurinic sites and 8-oxo-7,8-dihydroguanine bases at approximately 250bp resolution on a genome-wide scale. We directly demonstrate that the accumulation rate of apurinic sites varies widely across the genome, with hot spots acquiring many times more damage than cold spots. The experiment was performed in triplicates on HepG2 cells, 30 min after X-ray treatment (6Gy). AP-Seq is an approach that specifically enriches AP-sites via a biotin-labelled aldehyde-reactive probe under pH neutral conditions, which has been well established for the specific detection of AP-sites since its development by Kubo et al. in 1992. Under neutral conditions (pH7), 1h at 37ºC, the probe is highly specific for the aldehydes occurring at AP-sites. After biotin labelling of genomic DNA, DNA is sonicated into ~250 bp fragments, enriched, in vitro repaired (PreCR, NEB), and used for Illumina short read sequencing (125 bp, paired end, HiSeq2000). To assess oxidative damage as the sum of AP-sites and 8-oxoG, we applied recombinant OGG1 in vitro to the extracted DNA (OGG1-AP-seq). Under the conditions chosen, any remaining 8-oxoG is excised in a largely sequence-independent fashion after DNA extraction to result in a set of secondary AP-sites and to a lesser extent the associated beta-elimination product.

2018-10-22 | GSE121005 | GEO

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