Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell RNA-sequencing on aged mouse lung mesenchymal cells.

ABSTRACT: QC, integration, mesenchymal fraction extraction and purity confirmation were performed as described previously. The mesenchymal cell subpopulations identified in the aged normal and fibrotic lungs were similar to those identified in adult mouse lungs and each cluster showed a distinct gene expression profile.

ORGANISM(S): Mus musculus

PROVIDER: GSE157379 | GEO | 2021/06/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide analysis of gene expression in normal and fibrotic mouse kidneys and normal and fibrotic mouse lungs

Project description:In this study, adult virgin female BALB/C mice were kidney and lungs were harvested for RNA extraction (healthy kidney and lung). Adult virgin female BALB/C mice were subjected to unilateral ureter obstruction (UUO) to induce kidney fibrosis and the fibrotic kidney was harvested for RNA extraction. Adult virgin female BALB/C mice were subjected to intratracheal administration of bleomycine to induce lung fibrosis and the fibrotic lungs was harvested for RNA extraction.

2020-04-07 | GSE97546 | GEO

Identification of a Cell-of-Origin for Fibroblasts Comprising the Fibrotic Reticulum in Idiopathic Pulmonary Fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is a progressive disease of the middle aged and elderly with a prevalence of one million persons worldwide. The fibrosis spreads from affected alveoli into contiguous alveoli, creating a reticular network that leads to death by asphyxiation. Lung fibroblasts from patients with IPF have phenotypic hallmarks, distinguishing them from their normal counterparts: pathologically activated Akt signaling axis, increased collagen and a-smooth muscle actin expression, distinct gene expression profile, and ability to form fibrotic lesions in model organisms. Despite the centrality of these fibroblasts in disease pathogenesis, their origin remains uncertain. Here, we report the identification of cells in the lungs of patients with IPF with the properties of mesenchymal progenitors. In contrast to progenitors isolated from nonfibrotic lungs, IPF mesenchymal progenitor cells produce daughter cells manifesting the full spectrum of IPF hallmarks, including the ability to form fibrotic lesions in zebrafish embryos and mouse lungs, and a transcriptional profile reflecting these properties. Morphological analysis of IPF lung tissue revealed that mesenchymal progenitor cells and cells with the characteristics of their progeny comprised the fibrotic reticulum. These data establish that the lungs of patients with IPF contain pathological mesenchymal progenitor cells that are cells of origin for fibrosis-mediating fibroblasts. These fibrogenic mesenchymal progenitors and their progeny represent an unexplored target for novel therapies to interdict fibrosis.

2017-03-27 | GSE97038 | GEO

Characterization of young and aged lung tissue RNA 60 days post-influenza infection

Project description:To identify molecular characteristics of young and aged lungs post-influenza infection, we isolated RNA from lungs 60 days post-infection and examined by bulk RNAseq. We found a large number of genes remain upregulated in aged compared to young lungs. Comparison with expression of immune system-related genes from Nanostring expriments indicated this was largely infection-induced rather than baseline differences between age. This indicates that aged lungs fail to return to homeostasis following a viral respiratory infection

2020-10-06 | GSE159066 | GEO

Profiling of mesenchymal stem cells from adipose tissue of differentially aged mice

Project description:This SuperSeries is composed of the following subset Series: GSE25068: PcG/TrxG profiling of differentially aged adipose-derived mesenchymal stem cells GSE25069: Whole-genome microarray of long-term cultured adipose derived mesenchymal stem cells from differentially-aged mice GSE25679: microRNA profiling of mesenchymal stem cells from adipose tissue of differentially aged mice Refer to individual Series

2010-11-30 | E-GEOD-25685 | biostudies-arrayexpress

Comparative transcriptional analysis of lung fibroblasts from young and aged mice identifies PIM1/NFATc1 axis as a driver of persistent fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is an aging-associated disease characterized by the accumulation of myofibroblasts leading to the progressive scarring of the lung. To identify transcriptional gene programs driving persistent fibrosis in aged lungs, we performed a comparative RNA-seq analysis of fibroblasts freshly isolated from young and aged mouse lungs 30 days post-bleomycin injury. We discovered that lung fibroblasts isolated from young animals at this time point post-injury were transcriptionally similar to those isolated from uninjured mice. In contrast, aged lung fibroblasts isolated at the same time point exhibited a sustained pro-fibrotic state characterized by the elevated expression of genes implicated in inflammation, extracellular matrix remodeling, and cell survival. We identified the protein kinase pro-viral integration site of Moloney murine leukemia virus 1 (PIM1) and its direct target Nuclear Factor of Activated T Cells-1 (NFATc1) as putative drivers of the sustained profibrotic gene signatures observed in aged lung fibroblasts post-injury. PIM1 and NFATc1 transcripts were highly enriched in a pathogenic fibroblast population recently discovered in IPF lungs, and their protein expression was detected in fibroblastic foci. Overexpression of PIM1 in normal human lung fibroblasts potentiated their fibrogenic activation and this effect was dependent on NFATc1. Pharmacological inhibition of PIM1 in IPF-derived lung fibroblasts attenuated their activation and sensitized them to apoptotic stimuli. Finally, inhibition of PIM1 strongly reduced the expression of ECM remodeling and pro-survival genes and blocked the secretion of collagen in IPF lung explants ex vivo. Targeting PIM1/NFATc1 axis in pathogenic lung fibroblasts may represent a therapeutic strategy to limit their activation and promote fibrosis resolution in IPF.

2022-01-01 | GSE191208 | GEO

Pathogenesis of influenza A(H7N9) virus in aged non-human primates

Project description:The avian influenza A(H7N9) virus has caused high mortality in humans, especially in the elderly; however, little is known about the mechanistic basis for this. In this study, we employed non-human primates to evaluate the effect of aging on the pathogenicity of A(H7N9) virus. We observed that A(H7N9) virus infection of aged animals (defined as 20–26 years) caused more severe symptoms than infection of young animals (defined as 2 3 years). In aged animals, lung inflammation was weak and virus infection was sustained. Although cytokine and chemokine expression in the lungs of most aged animals was lower than that in the lungs of young animals, one aged animal showed dysregulated proinflammatory cytokine and chemokine production, resulting in it being euthanized. These results suggest that attenuated or dysregulated immune responses in aged animals are responsible for the severe symptoms observed among elderly patients infected with A(H7N9) virus.

2020-06-13 | GSE152406 | GEO

Single cell RNA sequencing of myeloid cells from lungs of young and aged mice

Project description:Single cell RNA sequencing from lungs of young (2-3 month old) and aged (20-22 month old) mice.

2021-10-20 | GSE167236 | GEO

Single-cell RNA-seq reveals fibroblast heterogeneity and increased mesenchymalfibroblastsin human skin fibrotic diseases

Project description:Skin fibrotic disease representsa major global healthcare burden, characterized by fibroblast hyperproliferation and excessive accumulation of extracellular matrix.Fibroblasts are found to be heterogeneous in multiple fibrotic diseases,but the fibroblast heterogeneity of skin fibrotic diseases remains unknown.In this study, we performed single-cell RNA-seq in keloid, a paradigm of skin fibrotic diseases, andnormal scardermis tissues.Our results indicate that keloid and normal scar fibroblasts could be divided into 4 subpopulations: secretory-papillary, secretory-reticular, mesenchymal and pro-inflammatory.The percentage of mesenchymal fibroblast subpopulationincreased significantly in keloid compared to normal scar. Interestingly, we also found increasing mesenchymal fibroblast subpopulation in scleroderma, another skin fibrotic disease.Function studies showed that the mesenchymal fibroblasts promoted collagen synthesis of the other fibroblasts in keloid partiallythrough secreting POSTN. These findings will help us understandskin fibroticpathogenesis in depth,and provided potential target cells for fibrotic diseases therapies.

2021-05-23 | GSE163973 | GEO

Single-cell RNA-seq reveals fibroblast heterogeneity and increased mesenchymal fibroblasts in human skin fibrotic diseases (RNA-seq)

Project description:Skin fibrotic disease representsa major global healthcare burden, characterized by fibroblast hyperproliferation and excessive accumulation of extracellular matrix.Fibroblasts are found to be heterogeneous in multiple fibrotic diseases,but the fibroblast heterogeneity of skin fibrotic diseases remains unknown.In this study, we performed single-cell RNA-seq in keloid, a paradigm of skin fibrotic diseases, andnormal scardermis tissues.Our results indicate thatkeloid and normal scar fibroblasts could be divided into 4 subpopulations: secretory-papillary, secretory-reticular, mesenchymal and pro-inflammatory.The percentage of mesenchymal fibroblast subpopulationincreased significantly in keloid compared to normal scar. Interestingly, we also found increasing mesenchymal fibroblast subpopulation in scleroderma, another skin fibrotic disease.Function studies showed that the mesenchymal fibroblasts promoted collagen synthesis of the other fibroblasts in keloid partiallythrough secreting POSTN. These findings will help us understandskin fibroticpathogenesis in depth,and provided potential target cells for fibrotic diseases therapies.

2021-06-01 | GSE175866 | GEO