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RNA-sequencing comparison of pneumonectomy and bleomycin reveals novel anti-fibrotic mechanisms and regulators

ABSTRACT: RNA-sequencing comparison of pneumonectomy and bleomycin reveals novel anti-fibrotic mechanisms and regulators

PROVIDER: PRJNA677893 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13040130_1.fastq.gz	Fastqsanger.gz
	SRR13040130_2.fastq.gz	Fastqsanger.gz
	SRR13040131_1.fastq.gz	Fastqsanger.gz
	SRR13040131_2.fastq.gz	Fastqsanger.gz
	SRR13040132_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

RNA-sequencing comparison of pneumonectomy and bleomycin reveals novel anti-fibrotic mechanisms and regulators

Project description:Fibroblast activation is transient in successful wound repair, but persistent in fibrotic pathologies. Understanding fibroblast deactivation during successful wound healing may provide new approaches to therapeutically reverse fibrogenic cell activation. To characterize the gene programs that accompany fibroblast activation and reversal during lung fibrosis resolution, we used RNA-seq analysis of flow-sorted Col1α1-GFP positive and CD45, CD31, and CD326 negative cells isolated from the lungs of young mice exposed to bleomycin and pneumonectomy. We compared fibroblasts isolated from controls to those isolated at days 14 and 30 after bleomycin exposure, as well as at 14 days after pneumonectomy, representing the peak of extracellular matrix deposition, early stage of fibrosis resolution, and non-fibrotic lung repair respectively.

2020-11-13 | GSE161322 | GEO

Transcriptomic changes of lung ECs following bleomycin induced pulmonary fibrosis, unilateral pneumonectomy, in WT mouse and the effect of Kitl deletion in Apln+ cells

Project description:To investigate transcriptomic changes of lung ECs following bleomycin induced pulmonary fibrosis and pneumonectomy, lung ECs from CT, Bleomycin induced model, and pneumonectomy model mouse were FACS sorted and single-cell RNA seqs were performed

2023-12-01 | GSE218972 | GEO

Transcriptional profile of mouse lung during the fibrotic phase of the response to bleomycin

Project description:Wildtype mice were given saline or bleomycin by oropharyngeal instillation. After 14 days, during the fibrotic phase of the response, lungs were dissected and total RNA was extracted and used for gene expression profiling. The aim was to identify those genes regulated during the development of fibrosis in this animal model of bleomycin-induced lung fibrosis. Wildtype male C57Bl/6J mice (8-10 weeks old) were used in the study, with three mice per group. Bleomycin (1mg/kg body weight in 50μl of saline) or saline was administered by oropharyngeal installation as described previously by Lakatos et al, Exp Cell Res, 2006, under light halothane-induced anaesthesia. After 14 days, lungs were removed, blotted dry and the trachea and major airways were excised before the separated lobes were snap frozen in liquid nitrogen. Lungs were then pulverized under liquid nitrogen, and the resulting lung powder was used for total RNA extraction using Trizol. Following DNase-treatment, clean-up, cDNA synthesis and cRNA synthesis, samples were hybridized to Affymetrix MOE430A genechips using standard protocols. The data were analyzed using RMA with quantiles normalization.

2009-07-07 | E-GEOD-16846 | biostudies-arrayexpress

Transcriptional profile of mouse lung during the fibrotic phase of the response to bleomycin

2009-07-07 | GSE16846 | GEO

The Anti-Fibrotic Drug Nintedanib Promotes Expansion of Lung Macrophages with a Distinct Transcriptional Repair Program in Bleomycin-Exposed Mice

Project description:Idiopathic pulmonary fibrosis (IPF) is a progressing chronic and fibrotic lung response with poor prognosis. The current standard-of-care for IPF is the kinase inhibitor nintedanib, which has a broad target range. The mechanism of nintedanib’s action remains unclear as it inhibits diverse kinases expressed in lung epithelia, endothelia and putatively the immune populations distributed throughout the lung. Given the proposed role of multiple pulmonary macrophage populations in mediating both protective and pathogenic roles in lung fibrosis, we sought to identify repair-associated macrophage populations in mice influenced by nintedanib after bleomycin challenge for 7 and 14 days using single cell RNA sequencing. Bleomycin exposure triggered expansion of inflammatory MHCIIhigh macrophage populations, which was partially reversed after nintedanib treatment. Concurrently, nintedanib promoted the expansion of MHCIIlow macrophages, which were linked to attenuation of lung fibrosis. Concomitantly, nintedanib promoted an increased expression of mRNA for canonical macrophage repair markers in MHCIIlow macrophages. Finally, exposure of inflammatory macrophages to nintedanib in vitro resulted in attenuation of expression of transcripts for MCHII. In conclusion, a component of nintedanib’s protective mode of action in lung fibrosis relies on expanding distinct MHCIIlow macrophage populations and redirecting them toward a reparative phenotype. This study provides a rationale for further refinement of therapeutic kinase inhibition in fibrotic diseases.

2021-05-05 | GSE151374 | GEO

RNA-seq profiling of ITPKC overexpression in normal human lung fibroblasts

Project description:Idiopathic pulmonary fibrosis (IPF) is characterized by pathogenic accumulation of scar tissue in the lung. Many of the processes implicated in fibrosis also occur following pneuomonectomy, but fibrotic changes are absent. We aimed to characterize differences between the responses to pneumonectomy and bleomycin, a fibrosis-inducing drug. We identified Itpkc as a gene uniquely up-regulated following pneumonectomy and identified it to have anti-fibrotic effects in cell culture. We then used RNA-sequencing on normal human lung fibroblasts overexpressing ITPKC or control to gain a deeper understanding of its role.

2023-12-06 | GSE220254 | GEO

Comparison of transcriptional changes in IPF mouse models (Bleomycin and Ad-TGFb)

Project description:Idiopathic Pulmonary Fibrosis (IPF) is a chronic, progressive, and often fatal disorder. Using an in-silico data-driven approach, we identified a robust connection between the transcriptomic perturbations in IPF disease and those induced by saracatinib, a selective Src kinase inhibitor, originally developed for oncological indications.We investigated the anti-fibrotic efficacy of saracatinib in two in vivo modeles (bleomycin and recombinant adenovirus transforming growth factor-beta (Ad-TGF-β) murine models of pulmonary fibrosis).

2022-08-30 | GSE178457 | GEO

Expression profiling PDE4B inhibitor BI 1015550 treatment in a therapeutic Rat Lung Bleomycin Model

Project description:Idiopathic pulmonary fibrosis (IPF) is a progressing chronic and fibrotic lung response with poor prognosis. To study the underlying molecular mechanisms of IPF, the rat bleomycin model is commonly used. Intratracheal application of bleomycin is known to induce inflammatory and fibrotic processes in the lung, e.g. infiltratin of inflammatory cells and collagen deposition. Recently, the PDE4B inhibitor BI 1015550 has been reported to prevent a decrease in lung function in patients with IPF. Here we examined the effect of PDE4 inhibitor BI 1015550 in the rat bleomycin model on transcriptional level by RNASeq.

2024-09-17 | GSE248263 | GEO

ChIP-seq of mouse alveolar organoids treated with bleomycin

Project description:In fibrotic lung, upregulation of p53 signaling in alveolar epithelium is observed. Then, we performed p53 ChIP-seq using alveolar organoids to investigate genes directly targeted by p53 protein in bleomycin-treated p53-upregulated alveolar epithelial cells.

2023-05-07 | GSE231445 | GEO

Expression data from mouse lung treated with saline or bleomycin

Project description:Lung fibrosis represents the final common pathway of a variety of lung injuries, and it is characterized, independently of etiology, by the expansion of the fibroblast/myofibroblast population and by the abnormal accumulation of extracellular matrix (ECM) replacing normal functional parenchyma. In general, there is no effective therapy, and currently the only helpful available treatment for advanced lung fibrosis is transplantation. In this study we aimed to document the time-related reversibility of bleomycin-induced lung fibrosis, and to determine the gene expression patterns associated with the initial progression and the subsequent regression of the fibrotic response by microarray in this bleomycin mouse model of lung fibrosis. Mice (C57BL/6 ) aging 8 to 10 weeks were instilled intratracheally with 0.10 U/10 g of bleomycin (Blenoxane, Bristol-Myers Squibb Co.) in 50 μl sterile saline. Control animals received an equal volume of sterile saline (9, 10). Mice were housed in specific pathogen-free conditions and provided with food and water ad libitum. All studies and procedures were approved by the Science and Ethic Committee at the National Institute of Respiratory Diseases and were performed according to the protocols and guidelines of the institutional animal care and use committee. Mice were sacrificed at 7 days and 1, 2, 3, and 4 months after bleomycin or saline treatment. For every variable, six control and six experimental mice were used.

2013-03-11 | E-GEOD-42301 | biostudies-arrayexpress

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