Murine model and pathogenesis of radiation induced liver fibrosis.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE179782 | GEO | 2022/06/22
REPOSITORIES: GEO
Similar Datasets
Project description:Murine model and pathogenesis of radiation induced liver fibrosis.
| PRJNA744929 | ENA
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: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:Radiation lung injury is characterized by early inflammation and late fibrosis. The causes underlying the chronic, progressive nature of radiation injury are poorly understood. Here, we report that the gene expression of irradiated lung tissue correlates with that observed in the lungs in aged animals. We demonstrate that NOX4 expression and superoxide elaboration is increased in irradiated lungs and pneumocytes in a dose dependent fashion. We used microarrays to detail the global programme of gene expression and report that irradiated lung tissue correlates with that observed in the lungs in aged animals. Female C57Bl/Ncr mice, aged 10 weeks were treated with/ without radiation to the thorax with a X-RAD 320 x-ray irradiator at a dose rate of 2.61 Gy/minute. An age-matched cohort of mice received no IR while additional cohorts received 5 Gy in a single dose, 17.5 Gy in a single dose. RNA was extracted and hybridization done on Affymetrix Mouse430_2 microarrays.
2013-11-01 | E-GEOD-41789 | biostudies-arrayexpress
Project description:Radiation lung injury is characterized by early inflammation and late fibrosis. The causes underlying the chronic, progressive nature of radiation injury are poorly understood. Here, we report that the gene expression of irradiated lung tissue correlates with that observed in the lungs in aged animals. We demonstrate that NOX4 expression and superoxide elaboration is increased in irradiated lungs and pneumocytes in a dose dependent fashion. We used microarrays to detail the global programme of gene expression and report that irradiated lung tissue correlates with that observed in the lungs in aged animals.
2013-11-01 | GSE41789 | GEO
Project description:Radiation-induced pulmonary fibrosis (RIPF) is the most common bottleneck of radiation therapy (RT) that limits its tumor-killing effect. Up to date, there is no effective therapeutic agent for RIPF treatment due to absence of realistic preclinical models. Lungs of mice exposed to focal, highly localized dose of 75Gy-100Gy represents short time-taking (up to 6 weeks) modality for mimicking recent advanced RT, stereotactic body RT-associated lung fibrosis. However, extensive fibrosis and possibility of animal lethality resulted from exposure to high dose raises a question regarding the appropriate dose threshold for limiting unnecessary responses and obtain clinically relevant results. We observed in preliminary trials that lung tissues of 65Gy-exposed mice are still able to develop inflammation and fibrosis at the same time cap. But the molecular changes associated with dose reduction is still unknown. To examine this, bulk RNA from 65Gy and 75Gy irradiated as well as normal lung tissues of mice were obtained, and analysed using computational approach to uncover the transcriptomal similarities and differences between the differentially irradiated samples. Differentially expressed genes (DEGs) were analysed and 2-week and 6-week intersected DEGs as well as 65 and 75Gy exclusive DEGs at 2-week and 6-week time points were detected using venn diagramme. Expression direction of intersected DEGs between 65Gy and 75Gy was checked and found to be consistent at both inflammation and fibrosis stages proven visually by MDS and heatmap graphs. All-times intersected DEGs are 488 and involved in inflammation, cytokine production, and cell proliferation; 2-week intersected DEGs are 221 and involved in cell cycle and DNA damage; 6-week intersected DEGs are 403 and involved in immunoglobin production, extracellular matrix (ECM) deposition, and ECM-receptor interactions. Interestingly, only 75Gy exclusive DEGs of 2 and 6 weeks presented inflammation and fibrosis-related biological process, respectively. These include anti-inflammatory process, cytokine production, EMT, vasculogenesis, and angiogenesis. These results suggested that 65Gy maybe a better dose for delivering less exaggerated, clinically relevant inflammation and fibrotic events, and thus, it can be utilised in establishing appropriate preclinical models for studying RIPF pathology and therapy.
2024-04-17 | GSE205025 | GEO
Project description:Normal lung tissue tolerance constitutes a limiting factor in delivering the required dose of radiotherapy to cure thoracic and chest wall malignancies. Patient genetic predisposition, the volume of irradiated lung and combination regimens consisting of concurrent chemotherapy are correlated with increased risk of radiation induced toxicity in lung. The main purpose of this study is to investigate dose-response regulations of fractionated (5-fractions) of mouse lung irradiation based on a comprehensive dose-escalation program, for a better understanding of molecular mechanism governing radiation induced lung fibrosis.
2022-08-02 | E-MTAB-5922 | biostudies-arrayexpress
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.
2023-03-20 | GSE211713 | GEO
Project description:PurposeFibrosis can be a disabling, severe side effect of radiotherapy that can occur in patients, and for which there is currently no effective treatment. The activins, proteins which are members of the TGFβ superfamily, have a major role in stimulating the inflammatory response and subsequent fibrosis. Follistatin is an endogenous protein that binds the activins virtually irreversibly and inhibits their actions. These studies test if follistatin can attenuate the fibrotic response using a murine model of radiation-induced fibrosis.Experimental designC57BL/6 mice were subcutaneously injected with follistatin 24 hours prior to irradiation. Mice were irradiated in a 10 x 10 mm square area of the right hind leg with 35 Gy and were given follistatin 24 hours before radiation and three times a week for six months following. Leg extension was measured, and tissue was collected for histological and molecular analysis to evaluate the progression of the radiation-induced fibrosis.ResultsLeg extension was improved in follistatin treated mice compared to vehicle treated mice at six months after irradiation. Also, epidermal thickness and cell nucleus area of keratinocytes were decreased by the follistatin treatment compared to the cells in irradiated skin of control mice. Finally, the gene expression of transforming growth factor β1 (Tgfb1), and smooth muscle actin (Acta2) were decreased in the irradiated skin and Acta2 and inhibin βA subunit (Inhba) were decreased in the irradiated muscle of the follistatin treated mice.ConclusionsFollistatin attenuated the radiation-induced fibrotic response in irradiated mice. These studies provide the data to support further investigation of the use of follistatin to reduce radiation-induced fibrosis in patients undergoing radiotherapy for cancer.
| S-EPMC5354399 | biostudies-literature