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A spatially restricted fibrotic niche in pulmonary fibrosis is sustained by M-CSF/M-CSFR signaling in monocyte-derived alveolar macrophages

ABSTRACT: A spatially restricted fibrotic niche in pulmonary fibrosis is sustained by M-CSF/M-CSFR signaling in monocyte-derived alveolar macrophages

PROVIDER: PRJNA525430 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8669100.fastq.gz	Fastqsanger.gz
	SRR8669101.fastq.gz	Fastqsanger.gz

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A spatially restricted fibrotic niche in pulmonary fibrosis is sustained by M-CSF/M-CSFR signaling in monocyte-derived alveolar macrophages

Project description:Pulmonary fibrosis is a heterogenous syndrome in which fibrotic scar replaces normal lung tissue. We performed single-cell RNA-seq on the lungs from mice exposed to fibrogenic particle (asbestos) and non-fibrogenic particle (TiO2) 14 days after the exposure to dissect cellular interactions unfolding during the early stages of the pulmonary fibrosis.

2019-09-26 | GSE127803 | GEO

Fibrotic Response to anti-CSF-1R Treatment Potentiates Glioblastoma Recurrence

Project description:Treatment of glioblastoma with anti-CSF-1R immunotherapy, radiotherapy, or surgical tumor resection were found to all induce a fibrotic response to treatment, which was highly associated with tumor recurrence. To investigate the drivers of fibrotic treatment response we performed multi-omic analysis of the glioblastoma microenvironment following treatment with anti-CSF-1R immunotherapy. Studies consisted of mass spectrometry proteomic analysis, single cell transcriptomics, and high-dimensional spatial analysis. These data identified a protective spatial niche that supported tumor cell survival following treatment, ultimately leading to tumor recurrence. Therapeutic inhibition of fibrotic treatment response blocked the formation of this niche, and significantly improved survival in anti-CSF-1R preclinical trials

2024-08-12 | PXD041689 | Pride

A spatially restricted fibrotic niche in pulmonary fibrosis is sustained by M-CSF/M-CSFR signalling in monocyte-derived alveolar macrophages.

Project description:Ontologically distinct populations of macrophages differentially contribute to organ fibrosis through unknown mechanisms.We applied lineage tracing, single-cell RNA sequencing and single-molecule fluorescence in situ hybridisation to a spatially restricted model of asbestos-induced pulmonary fibrosis.We demonstrate that tissue-resident alveolar macrophages, tissue-resident peribronchial and perivascular interstitial macrophages, and monocyte-derived alveolar macrophages are present in the fibrotic niche. Deletion of monocyte-derived alveolar macrophages but not tissue-resident alveolar macrophages ameliorated asbestos-induced lung fibrosis. Monocyte-derived alveolar macrophages were specifically localised to fibrotic regions in the proximity of fibroblasts where they expressed molecules known to drive fibroblast proliferation, including platelet-derived growth factor subunit A. Using single-cell RNA sequencing and spatial transcriptomics in both humans and mice, we identified macrophage colony-stimulating factor receptor (M-CSFR) signalling as one of the novel druggable targets controlling self-maintenance and persistence of these pathogenic monocyte-derived alveolar macrophages. Pharmacological blockade of M-CSFR signalling led to the disappearance of monocyte-derived alveolar macrophages and ameliorated fibrosis.Our findings suggest that inhibition of M-CSFR signalling during fibrosis disrupts an essential fibrotic niche that includes monocyte-derived alveolar macrophages and fibroblasts during asbestos-induced fibrosis.

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Spatially restricted immune and microbiota-driven adaptation of the gut

Project description:Spatially restricted immune and microbiota-driven adaptation of the gut

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Spatially restricted immune and microbiota-driven adaptation of the gut [scRNA-seq]

Project description:Spatially restricted immune and microbiota-driven adaptation of the gut [scRNA-seq]

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Project description:Spatially restricted immune and microbiota-driven adaptation of the gut [Spatial Transcriptomics]

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Spatially restricted position-dependent implications of lamin A promoter occupancy on gene activity (expression)

Project description:Interactions between the nuclear lamina (NL) and chromatin are thought to occur through large lamin association domains (LADs) and correlate with gene repression in these domains. We show that binding of lamin A/C (LMNA) to promoters occurs on discrete domains that are associated with distinct transcriptional outputs. Chromatin immunoprecipitation identifies thousands of LMNA-bound promoters, primarily linked to signaling functions. LMNA often occupies narrow domains on promoters, yet LMNA-bound promoters are often contiguous. LMNA-bound genes are overall repressed, but repression correlates with co-enrichment in repressive histone marks rather than LMNA occupancy per se. Genes marked by LMNA and H3K4me3 escape LMNA-associated repression in the absence of repressive histone marks. Positioning of LMNA on promoters relative to the TSS correlates with distinct transcriptional outputs: whereas upstream-distal binding can be transcriptionally permissive, TSS occupancy is associated with promoter inactivity. Perturbation in NL organization causes reorganization of lamin promoter occupancy and uncouples LMNA binding from promoter inactivity. Our results show the existence of many spatially restricted LMNA binding events on promoter regions, with distinct position-dependent transcriptional outputs. Total RNA obtained from ASCs and ASCs depleted of LMNA (LMNA-KD) and processed for microarray hybridization.

2013-07-14 | E-GEOD-42523 | biostudies-arrayexpress

CSF

Project description:CSF

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Spatially restricted position-dependent implications of lamin A promoter occupancy on gene activity (ChIPs and MeDips)

Project description:Interactions between the nuclear lamina (NL) and chromatin are thought to occur through large lamin association domains (LADs) and correlate with gene repression in these domains. We show that binding of lamin A/C (LMNA) to promoters occurs on discrete domains that are associated with distinct transcriptional outputs. Chromatin immunoprecipitation identifies thousands of LMNA-bound promoters, primarily linked to signaling functions. LMNA often occupies narrow domains on promoters, yet LMNA-bound promoters are often contiguous. LMNA-bound genes are overall repressed, but repression correlates with co-enrichment in repressive histone marks rather than LMNA occupancy per se. Genes marked by LMNA and H3K4me3 escape LMNA-associated repression in the absence of repressive histone marks. Positioning of LMNA on promoters relative to the TSS correlates with distinct transcriptional outputs: whereas upstream-distal binding can be transcriptionally permissive, TSS occupancy is associated with promoter inactivity. Perturbation in NL organization causes reorganization of lamin promoter occupancy and uncouples LMNA binding from promoter inactivity. Our results show the existence of many spatially restricted LMNA binding events on promoter regions, with distinct position-dependent transcriptional outputs. ChIPs were done from cultured untreated and LMNA-downregulated adipose stem cell (ASC) chromatin. MeDIPs were done from LMNA-downregulated ASCs. ChIP and MeDIP DNA was hybridized onto the aforementioned HG-18 Nimbegen promoter arrays.

2013-07-14 | E-GEOD-42522 | biostudies-arrayexpress

Spatially resolved RNA-sequencing of the embryonic zebrafish heart

Project description:Development of specialized cell types and structures in the vertebrate heart is regulated by spatially-restricted molecular pathways. Disruptions in these pathways can cause severe congenital cardiac malformations or functional defects. To better understand these pathways and how they regulate cardiac development and function we used tomo-seq, combining high-throughput RNA sequencing with tissue sectioning, to establish a genome-wide expression dataset with high spatial resolution for the developing zebrafish heart. Analysis of the dataset revealed over 1100 genes differentially expressed in sub-compartments. Pacemaker cells in the sinoatrial region induce heart contractions, but little is known about the mechanisms underlying their development and function. Using our transcriptome map, we identified spatially restricted Wnt/β-catenin signaling activity in pacemaker cells, which was controlled by Islet-1 activity. Moreover, Wnt/β-catenin signaling at a specific developmental stage in the myocardium controls heart rate by regulating pacemaker cellular response to parasympathetic stimuli. Thus, this high-resolution transcriptome map incorporating all cell types in the embryonic heart can expose spatially-restricted molecular pathways critical for specific cardiac functions.

2018-02-06 | GSE104057 | GEO

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