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Transcriptomic analysis of active form of Srebf1-overexpressed fibroblasts in bleomycin-induced lung fibrosis

ABSTRACT: Pulmonary fibrosis (PF) is an intractable disorder with a poor prognosis. Although lung fibroblasts play central roles in PF, their key regulatory molecules remain unclear. We performed transcriptome analysis of lung fibroblasts from bleomycin- and silica-treated murine lungs and identified 55 hub transcription factors highly connected to gene modules differentially expressed in PF. To elucidate whether fibroblast-specific intervention against the hub transcription factor Srebf1 modulates pathogenic activation of lung fibroblasts in vivo, we intratracheally-transferred active form of Srebf1-overexpressed fibroblasts into bleomycin-treated lungs and performed global transcriptome analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE110533 | GEO | 2019/01/30

REPOSITORIES: GEO

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Time-series transcriptomic analysis of lung fibroblasts in bleomycin- and silica-induced pulmonary fibrosis

Project description:Pulmonary fibrosis (PF) is an intractable disorder with a poor prognosis. Although lung fibroblasts play central roles in PF, their key regulatory molecules remain unclear. To identify PF pathology-associated gene modules and their hub TFs in activated lung fibroblasts, we performed time-course transcriptome analysis of the fibroblasts purified from the lungs of bleomycin- and silica-treated Col1a2-GFP reporter mice.

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Development of gene expression signatures for Mmp19 regulation of fibroblast phenotype in mouse lungs

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2014-08-05 | E-GEOD-49643 | biostudies-arrayexpress

Transcriptomic analysis of active form of Srebf1-overexpressed fibroblasts in bleomycin-induced lung fibrosis

Project description:Transcriptomic analysis of active form of Srebf1-overexpressed fibroblasts in bleomycin-induced lung fibrosis

| PRJNA433942 | ENA

Gene network analysis of interstitial macrophages after treatment with induced pluripotent stem cells secretome (iPSC-cm) in the bleomycin injured rat lung

Project description:Idiopathic pulmonary fibrosis (IPF) is a complex disease involving various cell types. Macrophages are essential in maintenance of physiological homeostasis, wound repair and fibrosis in the lung. Macrophages play a crucial role in repair and remodeling by altering their phenotype and secretory pattern in response to injury. The secretome of induced pluripotent stem cells (iPSC-cm) attenuates injury and fibrosis in bleomycin injured rat lungs. In the current study, we evaluate the effect of iPSC-cm on interstitial macrophage gene expression and phenotype in bleomycin injured rat lungs in vivo. Â iPSC-cm was intratracheally instilled 7 days after bleomycin induced lung injury and assessed 7 days later and single cell isolation was performed. Macrophages were FACS sorted and microarray analysis was performed. We characterized changes in the rat lung interstitial macrophages using transcriptional profiling.

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Project description:Pulmonary fibrosis (PF) is a chronic interstitial lung disease that causes irreversible and progressive lung scarring and respiratory failure. Activation of fibroblasts (FBs) play a central role in progression of PF. Here we report that platelet endothelial aggregation receptor 1 (Pear1) in FBs is a new molecular target for PF therapy. Pear1 deficiency spontaneously caused respiratory function decline and alveolar collagens accumulation in old mice. The degree of PF and mortality induced by bleomycin were significantly enhanced in Pear1 deficient mice. FB Mesenchyme-specific Pear1 deficiency aggravated bleomycin-induced PF, confirming that Pear1 modulates PF progression probably byvia regulation of FBs function. Single cell RNA-seq analysis of pulmonary FB and functional enrichment analysis revealed drastic expansion of Aactivated- FB clusters and enrichment of activated FB marker genes in extracellular matrix (ECM) development and pulmonary fibrosis in Pear1-/- fibrotic lungs. CD140+ bulk tissue RNA-seq analysis further confirmed that multiple mesenchyme development pathways especially epithelial mesenchymal transition (EMT) are enriched with up-regulated genes involving FB mediated ECM organization and development in in Pear1-/- fibrotic lungs. We further found that Pear1 associated with Protein Phosphatase 1 to suppress fibrotic factors such as TGFß, FGF or PDGF-induced intracellular signalling and FB activation. Intratracheal aerosolization of monoclonal antibody activating Pear1 greatly ameliorates PF in both wild-type mice and Pear1-humanized mice, suggesting that targeting Pear1 may serve as a new therapeutic strategy for PF.

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Monoclonal Antibody Targeting Pear1 for Pulmonary Fibrosis Therapy [bulk RNA-seq]

2021-10-20 | GSE183657 | GEO

Gene expression analysis of lung fibroblasts in bleomycin-induced pulmonary fibrosis

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2013-07-22 | E-GEOD-42564 | biostudies-arrayexpress

Single-cell RNA sequencing reveals profibrotic roles of three kinds of cells in pulmonary fibrosis

Project description:Pulmonary fibrosis (PF) is a serious chronic pulmonary disease, and lung transplantation is currently the only treatment option that can prolong patient survival. A greater understanding of the transcriptomes of cells related to the pathogenesis of PF can elucidate the impact of different cell types on its occurrence and development. To this end, we performed single cell RNA sequencing (scRNA-seq) to identify key cells and their biological processes in PF. We analyzed the transcriptomes of a total of 36400 cells isolated from the lungs of control and bleomycin-stimulated mice, and observed significant changes in the macrophages, fibroblasts and epithelial cells in the PF model. The macrophages were divided into alveolar macrophages (AMs) and interstitial macrophages (IMs). Based on the anatomical location, the fibroblasts were classified as alveolar fibroblasts, adventitial fibroblasts and peribronchial fibroblasts. Finally, the epithelial cells were divided into the type I alveolar epithelial cells, transitional type II alveolar epithelial cells, and Scgb3a2+ epithelial cells. The subgroups were further classified into key cell clusters to identify the signaling pathways involved in fibrotic progression. Finally, we identified several ligand-receptor complexes that mediate the communication between microphages, fibroblasts and epithelial cells during PF development. Our findings provide new insights into the mechanisms underlying PF, along with potential therapeutic targets.

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