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Multiome (GEX + ATAC) profile at single cell level of Foxf1 positive endothelial cells and mesenchymal cells from mouse lung at E18.5

ABSTRACT: Multiome (GEX + ATAC) profile at single cell level of Foxf1 positive endothelial cells and mesenchymal cells from mouse lung at E18.5

PROVIDER: PRJNA897893 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28424820_1.fastq.gz	Fastqsanger.gz
	SRR28424820_2.fastq.gz	Fastqsanger.gz
	SRR28424821_1.fastq.gz	Fastqsanger.gz
	SRR28424821_2.fastq.gz	Fastqsanger.gz
	SRR28424822_1.fastq.gz	Fastqsanger.gz

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Multiome (GEX + ATAC) profile at single cell level of Foxf1 positive endothelial cells and mesenchymal cells from mouse lung at E18.5

Project description:Foxf1 is enriched and differentially expressed in lung cells derived from mesoderm. We used single cell RNA sequencing (snRNAseq + snATAC) to analyze the dynamic transcriptional regulation in various lung cell types. The single cell analysis show the cell specific regulation of Foxf1 by distal enhancers that contribute to the molecular pathology of ACDMPV.

2024-04-01 | GSE217194 | GEO

Mouse embryonic lung FOXF1 ChIP-seq analysis

Project description:FOXF1 targets in embryonic day 18.5 mouse lungs were determined using FOXF1 immunoprecipitation followed by sequencing. FOXF1 binding sites in two biological replicates of pooled E18.5 wildtype mouse lungs (n=3) were to a 2% input control sample.

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Spatially resolved multiomics of human cardiac niches - Multiome GEX

Project description:Spatially resolved multiomics of human cardiac niches - Multiome GEX

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Spatially resolved multiomics of human cardiac niches - Multiome GEX

Project description:Using Multiome and previously published sc/snRNA-seq data, we studied eight anatomical regions of the human heart including left and right ventricular free walls (LV and RV), left and right atria (LA and RA), left ventricular apex (AX), interventricular septum (SP), sino-atrial node (SAN) and atrioventricular node (AVN). For the first time, we profile the cells of the human cardiac conduction system, revealing their distinctive repertoire of ion channels, G-protein coupled receptors and cell-cell interactions. We map the identified cells to spatial transcriptomic data to discover cellular niches within the eight regions of the heart.

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Foxf1 enchances pulmonary inflammation and mastocytosis

Project description:The Forkhead Box f1 (Foxf1) transcriptional factor (previously known as HFH-8 or Freac-1) is expressed in endothelial and smooth muscle cells in the embryonic and adult lung. To assess effects of Foxf1 during lung injury, we used CCl4 injury model. Foxf1+/- mice developed severe airway obstruction and bronchial edema, associated with increased numbers of pulmonary mast cells and increased mast cell degranulation following injury. Pulmonary inflammation in Foxf1+/- mice was associated with diminished expression of Foxf1, increased mast cell tryptase and increased expression of CXCL12, the latter being essential for mast cell migration and chemotaxis. Foxf1 haploinsufficiency caused pulmonary mastocytosis and enhanced pulmonary inflammation following chemically-induced lung injury, indicating an important role for Foxf1 in the pathogenesis of pulmonary inflammatory responses. Keywords: Influence of genetic modification on the pulmonary inflamation Foxf1+/- mice in which the Foxf1 allele was disrupted by an in-frame insertion of a nuclear localizing -galactosidase (-Gal) gene were bred for ten generations into the Black Swiss mouse genetic background. Carbon tetrachloride (CCl4; Sigma, St Louis, MO) was dissolved in mineral oil at a 1:20 ratio v/v and a single intraperitoneal (i.p.) injection of CCl4 (0.5 l of CCl4/ 1g of body weight) was administered to male Foxf1+/- mice or their wild type (WT) littermates as described.

2008-09-04 | E-GEOD-11112 | biostudies-arrayexpress

Foxf1 enchances pulmonary inflammation and mastocytosis

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Transcriptome analysis of FOXF1 expressing cells at E7.5 of embryonic development

Project description:Comparison of the transcriptional profile of cells expressing FOXF1::VENUS and/or FLK1 in E7.5 mouse embryos carrying a foxf1::venus knock-in allele

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FOXF1 transcription factor promotes lung regeneration after partial pneumonectomy

Project description:FOXF1, a member of the forkhead box family of transcription factors, has been previously shown to be critical for lung development, homeostasis, and injury responses. However, the role of FOXF1 in lung regeneration is unknown. Herein, we performed partial pneumonectomy, a model of lung regeneration, in mice lacking one Foxf1 allele in endothelial cells (PDGFb-iCre/Foxf1fl/+ mice). Endothelial cell proliferation was significantly reduced in regenerating lungs from mice deficient for endothelial Foxf1. Decreased endothelial proliferation was associated with delayed lung regeneration as shown by reduced respiratory volume in Foxf1-deficient lungs. FACS-sorted endothelial cells isolated from regenerating PDGFb-iCre/Foxf1fl/+ and control lungs were used for RNAseq analysis to identify FOXF1 target genes. Foxf1 deficiency altered expression of numerous genes including those regulating extracellular matrix remodeling (Timp3, Adamts9) and cell cycle progression (Cdkn1a, Cdkn2b, Cenpj, Tubb4a), which are critical for lung regeneration. Deletion of Foxf1 increased Timp3 mRNA and protein, decreasing MMP14 activity in regenerating lungs. ChIPseq analysis for FOXF1 and histone methylation marks identified DNA regulatory regions with the Cd44, Cdkn1a, and Cdkn2b genes, indicating they are direct FOXF1 targets. Thus FOXF1 stimulates lung regeneration following partial pneumonectomy via direct transcriptional regulation of genes critical for extracellular matrix remodeling and cell cycle progression.

2017-09-12 | GSE100149 | GEO

Forkhead Box F1 (FOXF1) represses fibroblast functions relevant to fibrogenesis

Project description:Aberrant expression of master phenotype regulators by lung fibroblasts may play a central role in idiopathic pulmonary fibrosis (IPF). Interrogating IPF fibroblast transcriptome datasets, we identified Forkhead Box F1 (FOXF1), a DNA-binding protein required for lung development, as a candidate actor in IPF. Thus, we determined FOXF1 expression levels in fibroblasts cultured from normal or IPF lungs in vitro, and explored FOXF1 functions in these cells using transient and stable loss-of-function and gain-of-function models. FOXF1 mRNA and protein were expressed at higher levels in IPF compared with controls. In normal lung fibroblasts, FOXF1 repressed key fibroblast functions such as proliferation, survival, and expression of collagen-1 (COL1) and actin related protein 2/3 complex, subunit 2 (ARPC2). ARPC2 knockdown mimicked FOXF1 overexpression with regard to proliferation and COL1 expression. FOXF1 expression was induced by the antifibrotic mediator prostaglandin E2 (PGE2). Ex vivo, FOXF1 knockdown conferred CCL-210 lung fibroblasts the ability to implant and survive in uninjured mouse lungs. In IPF lung fibroblasts, FOXF1 regulated COL1 but not ARPC2 expression. In conclusion, FOXF1 functions and regulation were consistent with an antifibrotic role in lung fibroblasts. Higher FOXF1 levels in IPF fibroblasts may thus participate in a compensatory response to fibrogenesis. Lung fibroblasts derived from 4 different IPF patients (P313, P355, P375 and P426) were transiently transfected with pcfoxf1 or control pcDNA3.1-constructs. Total RNAs were extracted 24 h after transfection and hybridized on microarrays. One color experiment with 2 experimental conditions: pcfoxf1 and pcDNA3.1

2014-10-01 | E-GEOD-52612 | biostudies-arrayexpress

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