Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1196531 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31680308_1.fastq.gz | Fastqsanger.gz | |||
| SRR31680308_2.fastq.gz | Fastqsanger.gz | |||
| SRR31680309_1.fastq.gz | Fastqsanger.gz | |||
| SRR31680309_2.fastq.gz | Fastqsanger.gz | |||
| SRR31680310_1.fastq.gz | Fastqsanger.gz |
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Project description:Radiation-induced pulmonary fibrosis (RIPF) is one of the most common side effects of lung cancer radiotherapy. In the mouse lungs developing RIPF, excessive accumulation of extracellular matrix and myofibroblasts with scar formation occurs. We used microarrays to detail the global program of gene expression underlying development of radiation-induced pulmonary fibrosis and identified a variety of genes whose expression were up-regulated during this process.
2017-01-12 | GSE93410 | GEO
Project description:Idiopathic pulmonary fibrosis (IPF) is an irreversible lung condition that progresses over time, which ultimately results in respiratory failure and mortality. In this study, we found that PLAC8 was downregulated in the lungs of IPF patients based on GEO data, in bleomycin (BLM)-induced lungs of mice, and in primary murine alveolar epithelial type II (pmATII) cells and human lung epithelial cell A549 cells. Overexpression of PLAC8 facilitated autophagy and inhibited apoptosis of pmATII cells and A549 cells in vitro. Moreover, inhibition of autophagy or overexpression of p53 partially abolished the effects of PLAC8 on cell apoptosis. ATII cell-specific overexpression of PLAC8 alleviated BLM-induced pulmonary fibrosis in mice. Mechanistically, PLAC8 interacts with VCP-UFD1-NPLOC4 complex to promote p53 degradation and facilitate autophagy, resulting in inhibiting apoptosis of alveolar epithelial cells and attenuating pulmonary fibrosis. In summary, these findings indicate that PLAC8 may be a key target for therapeutic interventions in pulmonary fibrosis.
2024-12-17 | GSE282477 | GEO
Project description:Radiation Induced Lung Injury (RILI) is one of the main limiting factors of thorax irradiation, which can induce acute pneumonitis as well as pulmonary fibrosis, the latter being a life-threatening condition. The order of cellular and molecular events in the progression towards fibrosis is key to the physiopathogenesis of the disease, yet their coordination in space and time remains largely unexplored. Here, we present an interactive murine single cell atlas of the lung responses to irradiation. This analysis opens the door for exploration of the spatio-temporal dynamics of the mechanisms that lead to radiation-induced pulmonary fibrosis. It depicts with unprecedented detail cell type-specific radiation-induced responses associated with either lung regeneration or the failure thereof. A better understanding of the mechanisms leading to lung fibrosis will help finding new therapeutic options that could improve patients’ quality of life.
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Project description:Expression data from radiation-induced pulmonary fibrosis mouse models
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Project description:Utilizing an established model of Radiation Induced Pulmonary Fibrosis, low input RNA sequencing was performed on whole lung cell suspensions obtained from 12.5 Gy thorax only radiation treated C57BL/6J mice and compareed to 0 Gy (Sham irradiation) age matched controls
2017-02-14 | GSE94852 | GEO
Project description:Objective:Biomarkers of radiation injury are needed in planning therapeutic measures for cancer patients receiving radiation therapy and civilians exposed to nuclear events. Previous research has highlighted the impact of radiation damage, with cancer patients developing acute disorders including radiation induced pneumonitis or chronic disorders including pulmonary fibrosis months after radiation therapy ends. Discovery of biomarkers that predict these injuries will offer the potential to treat people proactively to mitigate this damage and improve quality of life. Recent research has highlighted the potential for messenger RNA (mRNA), microRNA (miRNA), and long non-coding RNA (lncRNA) to be used as radiation biomarkers. Our study focused on the changes in these RNAs at 48h after radiation exposure of mouse lung tissue to define biological pathway changes and determine potential biomarkers. Result: We observed sustained dysregulation of specific mRNAs, lncRNAs, and miRNAs across all doses. We observed gene dysregulation which can be used to develop both markers to identify no-exposure vs radiation exposure including Hba and Hbb mRNA which were dysregulated even at 1 Gy. We also observed genes which can indicate high dose exposure including Cpt1c and Pdk4. Gdf15, and Eda2r, mRNA markers of senescence and fibrosis, were the most significantly upregulated. Only three miRNAs were significantly dysregulated across all radiation doses, with miRNA-142-3p and miRNA-142-5p downregulated and miRNA-34a-5p upregulated. IPA analysis indicated that numerous pathways relevant to immune function, cell proliferation and survival decreased with increasing doses of radiation. This data highlighted early pathways of dysregulation depending on dose of exposure. This data will help with development of treatments and in medical decision-making. Further experiments are planned to develop medical countermeasures based on this early dysregulation.
2022-06-06 | GSE202586 | GEO
Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic and often fatal pulmonary disorder characterized by fibroblast proliferation and the excess deposit of extracellular matrix proteins. The etiology of IPF is unknown, but a central role for microRNAs (miRNAs), a class of small non-coding regulatory RNAs, has been recently suggested. We report the upregulation of miR-199a-5p in mouse lungs undergoing bleomycin-induced fibrosis and also in human biopsies from IPF patients. Levels of miR-199a-5p were increased selectively in myofibroblasts and putative profibrotic effects of miR-199a-5p were further investigated in cultured lung fibroblasts. MiR-199a-5p expression was induced upon TGFβ exposure and ectopic expression of miR-199a-5p was sufficient to promote the pathogenic activation of pulmonary fibroblasts. CAV1, a critical mediator of pulmonary fibrosis, was established as a bona fide target of miR-199a-5p. Finally, we also found an aberrant expression of miR-199a-5p in mouse models of kidney and liver fibrosis, suggesting that dysregulation of miR-199a-5p represents a general mechanism contributing to the fibrotic process. We propose miR-199a-5p as a major regulator of fibrosis that represents a potential therapeutic target to treat fibroproliferative diseases. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2013-02-01 | E-GEOD-34818 | biostudies-arrayexpress
Project description:DNA damage and metabolic disorders are intimately linked with premature disease onset but the underlying mechanisms remain poorly understood. Persistent DNA damage accumulation in tissue-infiltrating macrophages carrying an ERCC1-XPF DNA repair defect (Er1F/-) riggers Golgi dispersal, dilation of endoplasmic reticulum, autophagy and exosome biogenesis leading to the secretion of extracellular vesicles (EVs) in vivo and ex vivo.
2019-11-04 | E-MTAB-8439 | biostudies-arrayexpress
Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, irreversible, and lethal lung disease. The initiation of IPF involves microinjuries to and/or dysfunction of the alveolar epithelium, but factors that determine fibrosis progression or normal tissue repair are largely unknown. We previously demonstrated that autophagy inhibition-mediated epithelial-mesenchymal transition (EMT) in human alveolar epithelial type II (ATII) cells augments local myofibroblast differentiation in pulmonary fibrosis by paracrine signalling. Here, we report that liver kinase B1 (LKB1) inactivation in ATII cells induces autophagy inhibition and EMT as a consequence. In IPF lungs, this is caused by a downregulation of CAB39L, a key subunit within the LKB1 complex. 3D co-cultures of ATII cells and lung fibroblast MRC5 coupled with RNA sequencing (RNA-seq) confirmed that paracrine signalling between LKB1-depleted ATII cells and fibroblasts augmented myofibroblast differentiation. Together these data suggest that reduced autophagy caused by LKB1 inhibition can induce EMT in ATII cells and contribute to fibrosis via aberrant epithelial–fibroblast crosstalk.
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