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Project description:Effect of Fibrosis in FMO3 Knockout Mice in a bleomycin-induced fibrosis Model
| PRJNA1455610 | ENA
Project description:Bleomycin-induced pulmonary fibrosis in mice mimics major hallmarks of idiopathic pulmonary fibrosis, yet in this model it spontaneously resolves over time. We studied molecular mechanisms of fibrosis resolution and lung repair, focusing on transcriptional and proteomic signatures and the effect of aging. Young (3 months) and old (21 months) mice were treated with Bleomycin or with control saline solution and analyzed transcript and protein expression over 8 weeks (Day 0, 14, 21, 28, 35, 42, 49, 56).
2024-09-10 | PXD040530 | Pride
Project description:Bleomycin-induced pulmonary fibrosis in mice mimics major hallmarks of idiopathic pulmonary fibrosis, yet in this model it spontaneously resolves over time. We studied molecular mechanisms of fibrosis resolution and lung repair, focusing on transcriptional and proteomic signatures and the effect of aging. Young (3 months) and old (21 months) mice were treated with Bleomycin or with control saline solution and analyzed transcript and protein expression over 8 weeks (Day 0, 14, 21, 28, 35, 42, 49, 56).
2023-08-09 | PXD041050 | Pride
Project description:To investigate the role of Dectin-1 in the development of pulmonary fibrosis, we used Dectin-1-deficient (Clec7a–/–, KO) mice to establish a bleomycin-induced pulmonary fibrosis model and compared it with WT mice.
2025-07-01 | GSE279043 | GEO
Project description:Intratracheal application of bleomycin is known to induce inflammatory and fibrotic reactions in the lung within a short period of time and histological features include infiltration of inflammatory cells, collagen deposition and obliteration of alveolar spaces. Because some of these features are found in patients with idiopathic pulmonary fibrosis (IPF), the bleomycin-induced lung fibrosis animal model is commonly used. However, exploratory treatments that were successfully used in this animal model and progressed to clinical trials lacked significant efficacy in humans. Here, the bleomycin-induced rat lung fibrosis model was studied using whole genome expression data that was collected at various time points and the relevance to human disease was evaluated through comparison with whole genome expression data from IPF patient-derived lung biopsies. The highest gene expression correlation between both species was observed in animals 7 days after bleomycin instillation. These gene expression signatures helped to identify a set of twelve novel disease-relevant translational gene markers that were able to separate IPF patients from controls. Furthermore, three Wnt/-catenin pathway-related genes that belong to this translational gene marker set showed, together with clinical diffusing capacity of the lung for carbon monoxide (DLCO) measurements, the potential to stratify IPF patients according to disease severity. Pirfenidone attenuated a subset of the translational gene markers in the bleomycin-induced fibrosis model, in particular those related to Wnt/-catenin-signaling. This novel translational gene marker panel offers improved possibilities to evaluate disease-modifying efficacy of novel therapeutic concepts in the bleomycin-induced rat lung fibrosis model and could be applied as a diagnostic and prognostic tool for IPF patient care. Comparison of bleomycin-treated and control rats after 3 days, 1 week, 2 weeks, 3 weeks, 4 weeks, 6 weeks and 8 weeks; 5 animals per group
2014-10-28 | E-GEOD-48455 | biostudies-arrayexpress
Project description:We purposed to examine the effect of PGF receptor FP in development of ; bleomycin-induced pulmonary fibrosis in mice. We performed gene ; expression analysis in the lung of WT and FP-KO mice on Days 0, 7 and ; 14. We found out that fibrosis-related genes such as various isoforms ; of collagen, which were induced on Day 7 and continued to increase or ; remained unchanged on Day 14, were induced to less extent in FP-KO ; mice. In contrast, expression of inflammation-related genes peaked on ; Day 7 similarly in WT and FP-KO mice. These results suggest that FP ; functions in fibrosis-phase, not in peak inflammation phase, and ; facilitates fibrogenesis by enhancing expression of fibrosis-related ; genes. Experiment Overall Design: RNA was prepared from the lung of WT and FP-KO mice on Day 0, 7 and 14 Experiment Overall Design: (n=4-5 for each group at each time point) after bleomycin instillation, Experiment Overall Design: and used for hybridization with Affymetrics mouse 430 2.0 microarrays. Experiment Overall Design: Time-dependent changes in expression of genes in FP-KO mice were Experiment Overall Design: compared with those in WT mice.
2009-11-11 | E-GEOD-18800 | biostudies-arrayexpress
Project description:The molecular mechanisms of lung injury and fibrosis are incompletely understood. microRNAs (miRNAs) are crucial biological regulators by suppression of their target genes and are involved in a variety of pathophysiologic processes. To gain insight into miRNAs in the regulation of lung fibrosis, total RNA was isolated from lung samples harvested at different days after bleomycin treatment, and miRNA array was performed thereafter. miRNAs expressed in lungs with bleomycin treatment at different time points were compared to miRNAs expressed in lungs without bleomycin treatment, resulting in 161 miRNAs differentially expressed. Furthermore, miRNA expression patterns regulated in initial and late periods after bleomycin were identified. Target genes were predicted in silico for differentially expressed miRNAs, including miR-7f, miR-7g, miR-196b, miR-16, miR-195, miR-25, miR-144, miR-351, miR-34a, miR-499, miR-704, miR-717, miR-10a, miR-211, miR-34a, miR-367 and miR-21, and then cross-referenced to molecular pathways including apoptosis, Wnt, Toll-like receptor, and TGF-? signaling, which are involved in different pathological phenotypes such as apoptosis, inflammation, and fibrosis. Our study demonstrated relative abundance of miRNA levels in bleomycin-induced lung fibrosis. The miRNAs and their potential target genes identified herein contribute to the understanding of the complex transcriptional program of lung fibrosis. Under anesthesia, 2.5 U/kg bleomycin dissolved in sterile PBS was administered via trachea as previously described. Lung tissues were harvested at the time point of day 0, 3, 7, 14, and 21 post bleomycin challenges. 3 sample in specific time point, except for day 14 where nday14 = 2.
2012-04-12 | E-GEOD-24323 | biostudies-arrayexpress
Project description:INTRODUCTION: Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with a poor prognosis, causing irreversible lung parenchymal damage. Pirfenidone and nintedanib exhibit some benefits on IPF, although they cannot cure or reverse its progression. Moreover, the molecular mechanisms responsible for their effects remain not entirely comprehended. Nintedanib, a multi-kinase receptor modulator, suppresses diverse proliferative pathways and displays antifibrotic effects in lung fibrosis models. However, the effects of its administration on the lung transcriptome have not yet been deeply investigated in in vivo models of lung fibrosis. This study aims to assess nintedanib's comprehensive transcriptomic profile in a rat model of bleomycin-induced lung fibrosis. MATERIALS & METHODS: Lung fibrosis was induced by two intratracheal administrations of bleomycin. Nintedanib “curative” protocol included three weeks of daily oral treatments (100 mg/kg) beginning seven days after the first bleomycin dose. At the end of the experiment, left lungs were processed for histological fibrosis evaluation by using an automated quantification system and the Ashcroft Score assessment. Right lungs were employed for RNA sequencing to undertake Differential Expression Analysis (DEGs) and a correlation network analysis (WGCNA). WGNA modules were thoroughly examined by cell and pathway enrichment analysis. Moreover, lipid peroxidation was assessed through the measurement of malondialdehyde (MDA) amount in right lung lysates. RESULTS: Bleomycin induced significant fibrotic lesions, as confirmed by the automated quantification and the Ashcroft Score. Nintedanib reduced the size of fibrotic lesions (≃15%) and the incidence of severe Ashcroft scores. The number of differentially expressed genes decreased from over 2000 in fibrotic animals to barely more than 400 in nintedanib-treated rats, when compared to controls. WGCNA identified two gene clusters correlated to histological parameters, both characterized by gene expression patterns where nintedanib-treated animals resemble the profile observed in control animals. One cluster was associated with mesenchymal cells and focused on epithelial to mesenchymal transition and extracellular matrix organization pathways, in line with the exhibited anti-fibrotic effect of nintedanib. The second cluster, involving resident macrophages and inflammatory pathways, was specifically related to lipid homeostasis, potentially uncovering a new mechanistic role of nintedanib in modulating lung fibrosis. CONCLUSIONS: The mechanisms involving macrophages and lipid metabolism, both of which were influenced by nintedanib treatment in this in vivo study, may open new research directions to better inquire about the role of this cellular type in the regulation of lipid homeostasis and fibrosis, influencing both tissue repair and pathological lung fibrosis.
2026-02-12 | GSE278200 | GEO
Project description:Genomic profiling of bleomycin- and saline-treated mice across 7 timepoints (1, 2, 7, 14, 21, 28, 35 days post treatment) was carried out in C57BL6/J mice to determine the phases of response to bleomycin treatment which correspond to onset of active pulmonary fibrosis. Temporal genomic characterization of lung homogenate from male C57BL6/J mice treated intratracheally with bleomycin or saline was carried out at 7 timepoints post treatment (1, 2, 7, 14, 21, 28, 35 days). Bleomycin (2U/kg) in 50 μl was intratracheally sprayed once into mice lightly anaesthetized with isoflurane (5% in 100% O2). Control animals received 50 μl of saline. Total RNA was isolated from the mouse lung tissue of bleomycin- and saline-treated mice across the 7 time points (n=8 per group) and homogenized in QIAzol reagent. Purified total RNA was amplified and labeled using NuGen Ovation kits (NuGEN Technologies, Inc., San Carlos, CA), and RNA from samples was hybridized to Affymetrix Mouse 430 2.0 arrays. One sample (saline treated, d14) was flagged as an outlier in principal component analysis and removed from subsequent analysis.
2013-04-10 | E-GEOD-40151 | biostudies-arrayexpress
Project description:Investigation of whole genome gene expression level changes in Bleomycin induced pulmonary fibrosis mouse model lung tissue, compared to the Sham group.
2017-01-20 | GSE77326 | GEO