Bisphenol AP promotes the development of bleomycin-induced pulmonary fibrosis by regulating macrophage function
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PROVIDER: PRJNA1220195 | ENA |
REPOSITORIES: ENA
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Project description:Bisphenol AP (BPAP), a structural analogue of bisphenol A (BPA), has been frequently detected in humans. The presence of BPAP is linked to various adverse health outcomes, including metabolic diseases and mood disorders. However, the effects by which BPAP contributes to lung diseases remain inadequately understood. This study utilized the mouse macrophage cell line RAW 264.7 and bleomycin induced pulmonary fibrosis model (PF) of C57BL/6 mice to explore the effects of BPAP. Functional experiments demonstrated that BPAP exposure inhibited macrophage proliferation and enhanced oxidative stress. Additionally, BPAP exposure enhanced the phagocytic and chemotactic functions of macrophages.
2025-08-21 | GSE288992 | GEO
Project description:Pulmonary fibrosis is a disease characterized by inflammatory cell infiltration, scar formation, deposition of extracellular matrix, alveolar epithelial cell injury and hyperplasia. To determine if alterations in microRNA expression contribute to these phenotypes, microRNA expression profiling of the lungs from bleomycin treated C57Bl/6J mice, relative to that of untreated controls, was undertaken. Mice were treated at 8 weeks old with 100 Units/kg of bleomycin delivered subcutaneously with osmotic minipumps. At 42 days post treatment mice were euthanized and lung microRNA isolated. We identified 11 microRNA's to be significantly differentially expressed (FDR threshold of 0.01) in the lungs of bleomycin treated mice and confirmed these data with real time PCR measurements. These included bleomycin upregulated miR-34a, 335-5p, 207, 21, 301a, 146b, 199a-5p, and 449a and bleomycin downregulated miR-151-3p, 26a and 676. We have previously shown that 1558 genes are differentially expressed in the lungs of bleomycin treated mice. Of the 1412 targets of upregulated microRNAs, 142 were confirmed to be downregulated in the gene expression profile (GEP). Of the 583 targets of downregulated microRNAs, 53 were confirmed to be upregulated in the gene expression profile. Pathway analysis of the microRNA targets and GEP overlapping genes indicated that altered microRNA expression is associated with cellular development, cellular growth, cellular proliferation and changed tissue/cell morphology. Specific pathways include HGF signaling, Cholecystokinin/Gastrin-mediated signaling, Endothelin-1 signaling, RAR activation, Phospholipase C signaling and IGF1 signaling. We conclude that altered microRNA expression is a feature of pulmonary fibrosis which putatively influences components of the altered airway disease. Two condition study, C57Bl/6J mice treated with 100 Units/kg bleomycin and untreated controls. Biological replicated n =3 for each group. Left lung tissue.
2013-09-01 | E-GEOD-45789 | biostudies-arrayexpress
Project description:We conducted fibroblast-specific transcriptome analysis by next generation sequencing in order to investigate qualitative change and activation signatures of lung fibroblasts in bleomycin-induced pulmonary fibrosis. Lung fibroblasts were identified by using reporter mice of collagen-α2(I), in which collagen I-producing fibroblasts were labeled with EGFP. Lungs were dissociated with protease sollution, and single cell suspension were stained with lineage markers (Ter119, CD45, CD31, EpCAM). Lineage- GFP+ cells were sorted out and mRNA was collected. Using serial analysis of gene expression (SAGE) method, we identified 2,973,937 SAGE tags (1,080,798 tags from saline-treated GFP+ fibroblasts and 1,893,139 tags from bleomycin-treated GFP+ fibroblasts). We found that genes related to extracellular matrix construction were highly up-regulated in fibroblasts from belomycin-treated lungs. Moreover, an analysis of mRNA profiles revealed biological functions such as proliferation, invasion, adhesion, and migration were promoted in fibroblasts from bleomycin-treated lung, which recapitulated the role of fibroblasts in the fibrogenesis. These fibroblast-specific gene expression profiles will be important notions in future fibrosis studies. mRNA profiles of Lung fibroblasts from 3 mice at day 14 after saline or bleomycin treatment.
2013-07-22 | E-GEOD-42564 | 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
Project description:Pulmonary fibrosis is a disease characterized by inflammatory cell infiltration, scar formation, deposition of extracellular matrix, alveolar epithelial cell injury and hyperplasia. To determine if alterations in microRNA expression contribute to these phenotypes, microRNA expression profiling of the lungs from bleomycin treated C57Bl/6J mice, relative to that of untreated controls, was undertaken. Mice were treated at 8 weeks old with 100 Units/kg of bleomycin delivered subcutaneously with osmotic minipumps. At 42 days post treatment mice were euthanized and lung microRNA isolated. We identified 11 microRNA's to be significantly differentially expressed (FDR threshold of 0.01) in the lungs of bleomycin treated mice and confirmed these data with real time PCR measurements. These included bleomycin upregulated miR-34a, 335-5p, 207, 21, 301a, 146b, 199a-5p, and 449a and bleomycin downregulated miR-151-3p, 26a and 676. We have previously shown that 1558 genes are differentially expressed in the lungs of bleomycin treated mice. Of the 1412 targets of upregulated microRNAs, 142 were confirmed to be downregulated in the gene expression profile (GEP). Of the 583 targets of downregulated microRNAs, 53 were confirmed to be upregulated in the gene expression profile. Pathway analysis of the microRNA targets and GEP overlapping genes indicated that altered microRNA expression is associated with cellular development, cellular growth, cellular proliferation and changed tissue/cell morphology. Specific pathways include HGF signaling, Cholecystokinin/Gastrin-mediated signaling, Endothelin-1 signaling, RAR activation, Phospholipase C signaling and IGF1 signaling. We conclude that altered microRNA expression is a feature of pulmonary fibrosis which putatively influences components of the altered airway disease.
2013-09-01 | GSE45789 | 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. Old mice showed delayed and incomplete lung function recovery 8 weeks after Bleomycin instillation. This shift in structural and functional repair in old Bleomycin-treated mice was reflected in a temporal shift in gene and protein expression. We reveal gene signatures and signaling pathways which underpin the lung repair process.
2023-10-16 | GSE218997 | 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:Selinexor is an orally bioavailable, small-molecule selective inhibitor of nuclear export protein that has been approved for the clinical treatment of relapsed or refractory multiple myeloma. At present, some studies have found that Selinexor can play an anti-inflammatory role in sepsis. We found that Selinexor, a selective inhibitor of XPO1, can alleviate bleomycin-induced pulmonary fibrosis in mice in our research work, but the specific mechanism is still unclear. After Selinexor treatment of bleomycin-induced pulmonary fibrosis in mice, we detected some differentially expressed proteins through proteomics, which may be the key mechanism of alleviating pulmonary fibrosis.
2023-08-01 | PXD044259 |
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: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.
2013-04-10 | GSE40151 | GEO