Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gli1+ cells in bone marrow fibrosis

ABSTRACT: Gli1+ cells as a driver and key target in bone marrow fibrosis

PROVIDER: PRJEB19811 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR1865250_1.fastq.gz	Fastqsanger.gz
	ERR1865250_2.fastq.gz	Fastqsanger.gz
	ERR1865251_1.fastq.gz	Fastqsanger.gz
	ERR1865251_2.fastq.gz	Fastqsanger.gz
	ERR1865252_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Characterization of murine non-hematopoietic Gli1+ bone marrow cells in homeostasis

Project description:We performed fate tracing of Gli1+ cells in homeostasis. Sorted cells were subjected to scRNAseq and integrated with non-hematopoietic cells from mice with myelofibrosis induced by either ThPO- or JAK2V617F-overexpression. Gli1+tdTom+ cells largely overlap with pro-fibrotic adipogenic and osteogenic MSCs, which show a strong upregulation of ECM related transcripts. Additionally, a subgroup of Gli1+tdTom+ cells shows similarity with bone marrow SCPs.

2020-11-03 | GSE156440 | GEO

GLI1+ mesenchymal stromal cells modulate epithelial metaplasia in lung fibrosis

Project description:A single-cell transcriptional analysis was performed on GLI1+ stromal cells from the adult murine lung during homeostasis and after fibrotic injury. The goal is to understand the role of GLI1+ stromal cells in lung fibrosis and repair. Whole adult murine lung tissue from two samples were separately dissociated to single cells and subjected to fluorescence activated cell sorting (FACS) to select all live GLI1+ cells. One sample was treated with bleomycin to induce fibrosis and the other was treated with saline as a control. The single cell RNA-sequencing library was generated separately for the bleomycin and saline-treated samples. Cells were sequenced at a depth of ~70,000 reads/cell. We captured approximately 17,700 cells with a median of 2,400 genes detected per cell utilizing a droplet-based barcoding approach to capture single cells for RNA sequencing. After bleomycin-induced fibrosis, we identified a novel "myofibroblast" subset of GLI1 cells that contribute to injury and repair. Injured GLI1 cells also reveal dysregulation in key developmental pathways, including BMP signaling, that contribute to metaplastic repair after fibrotic injury.

2020-08-17 | GSE140032 | GEO

Characterization of murine non-hematopoietic Gli1+ bone marrow cells in homeostasis

Project description:Characterization of murine non-hematopoietic Gli1+ bone marrow cells in homeostasis

| PRJNA657885 | ENA

CXCL4 and bone marrow fibrosis

Project description:Understanding the role of CXCL4 in the initiation and progression of bone marrow fibrosis

| PRJEB39607 | ENA

Endothelial LATS2 is a suppressor of bone marrow fibrosis

Project description:Endothelial LATS2 is a suppressor of bone marrow fibrosis

| PRJNA935694 | ENA

Endothelial LATS2 is a suppressor of bone marrow fibrosis

Project description:The skeletal system vasculature and specialized capillary subtypes regulate crucial elements of bone growth and regeneration. However, little is known about endothelial cell (EC) activation and plasticity during bone remodeling. Here, we demonstrate that the inactivation of the gene encoding Hippo kinase large tumor suppressor kinase 2 (Lats2) in ECs results in the development of a vascular defect in the metaphysis, which favours accumulation of hypertrophic chondrocytes and induces bone marrow fibrosis in the bone.

2024-06-03 | GSE225429 | GEO

Bone Marrow Transplantation in Treating Patients With Hematologic Cancer

Project description:RATIONALE: Radiation therapy uses high-energy x-rays to damage cancer cells. Drugs used in chemotherapy use different ways to stop cancer cells from dividing so they stop growing or die. Combining chemotherapy with bone marrow transplantation may allow the doctor to give higher doses of chemotherapy drugs and kill more tumor cells. PURPOSE: Phase II trial to study the effectiveness of bone marrow transplantation in treating patients who have hematologic cancer.

| 2004880 | ecrin-mdr-crc

An ageing bone marrow exacerbates lung fibrosis via a dysregulated regulatory T cell driven axis, fuelling profibrotic macrophage persistence

Project description:Pulmonary fibrosis is an incurable disease, which increasingly manifests with advanced age. Yet, how the ageing hematopoietic niche influences immune cell function and fibrosis progression in the lungs remains elusive. Using heterochronic transplant mouse models, we discovered that an aged bone marrow exacerbates lung fibrosis irrespective of lung tissue age. Upon lung injury, there was an increased pulmonary infiltration of monocyte-derived alveolar macrophages (Mo-AMs) from an aged bone marrow. These Mo-AMs displayed an enhanced profibrotic profile and a delayed transition in acquiring a homeostatic tissue-resident phenotype. This impaired Mo-AM differentiation was attributed to diminished numbers of regulatory T cells (Tregs) and the reduced availability of the anti-inflammatory cytokine IL-10 in the lung microenvironment of mice engrafted with aged bone marrow. Mechanistically, we show that Tregs are crucial providers of IL-10 that promote timely Mo-AM maturation and attenuate fibrosis progression. Our findings demonstrate the critical influence of an aged bone marrow on the development of lung fibrosis and identify a Treg-mediated resolutory axis as a potential therapeutic target for accelerated tissue repair.

2024-12-16 | GSE277799 | GEO

An ageing bone marrow exacerbates lung fibrosis via a dysregulated regulatory T cell driven axis, fuelling profibrotic macrophage persistence.

2024-12-02 | GSE274253 | GEO

Bone marrow niche

Project description:Bone marrow niche

| PRJNA429031 | ENA