Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA962191 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression analysis of bleomycin induced pulmonary fibrosis mouse model lung tissues
| PRJNA310060 | ENA
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
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
Project description:Idiopathic pulmonary fibrosis is a chronic devastating disease of unknown etiology. No therapy is currently available. A growing body of evidence supports the role of TGFβ1 as the major player in the pathogenesis of the disease. This study designed novel human- and mouse-specific siRNAs and siRNA/DNA chimeras targeting both human and mouse common sequences and evaluated their inhibitory activity in pulmonary fibrosis induced by bleomycin and lung-specific transgenic expression of human TGFβ1. Selective novel sequences of siRNA and siRNA/DNA chimeras efficiently inhibited pulmonary fibrosis, indicating their applicability as tools for treating fibrotic disease in humans. Total RNA was extracted from lung tissue from mice with bleomycin (BLM)-induced lung fibrosis treated with mouse TGFβ1 siRNAs or vehicle on different days after BLM infusion.
2011-11-22 | E-GEOD-28122 | biostudies-arrayexpress
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:Analysis of whole genome gene expression levels in distal lung tissue from mice with systemically bleomycin-induced pulmonary fibrosis. The hypothesis is that bleomycin promotes a specific genotype associated with development of pulmonary fibrosis and that treatment with compound EXT reduces the induction of genes related to the early progression of fibrosis.
2017-09-06 | GSE103511 | GEO
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:We have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish Mmp19 regulation of fibroblast phenotype changes in mouse lungs. Pulmonary fibrosis was induced by bleomycin at 0.08 u in 50ul of saline. At 21st day the mice were sacrificed and mouse lung fibroblasts were isolated and cultured in FBM plus additives following Lonza's portocol. RNA was extracted with miRNA mini kit from Qiagen. Gene expression microarray was performed with Agilent. A 834-gene consensus signature was identified that distinguished between Mmp19 knockout mice from wildtype. Some gene expression in the same RNA samples were validtaed by real-time PCR. The established bleomycin induced fibrosis was used in this experiment. At day 21 the fibrosis would be the situation of stable fibrosis. We administrated 0.08u of bleomycin intratracheally into wildtype and Mmp19 knockout mice, sacrificed the mice at 21st day and isolated the lung fibroblasts and culturing. Five independent experiments were performed and 3 for gene expression experiment.
2014-08-05 | E-GEOD-49643 | biostudies-arrayexpress
Project description:The most preclinical used in vivo model to study lung fibrosis is the bleomycin-induced lung fibrosis model in 2-3-month-old mice. Although this model resembles key aspects of idiopathic pulmonary fibrosis (IPF), there are limitations in its predictability for the human disease. One of the main differences is the juvenile age of animals that are usually used in experiments, resembling humans of around 20 years. Because IPF patients are usually older than 60 years, aging appears to play an important role in the pathogenesis of lung fibrosis. We here compared young (3 months) and old (21 months) mice 21 days after intratracheal bleomycin instillation.
2024-09-10 | PXD026222 | Pride