Induced Torpor: An Experimental Model to Investigate the Effects of Chronic Low-Dose Radiation Exposure on Zebrafish Liver
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ABSTRACT:
PROVIDER: PRJNA823689 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18645014_1.fastq.gz | Fastqsanger.gz | |||
| SRR18645014_2.fastq.gz | Fastqsanger.gz | |||
| SRR18645015_1.fastq.gz | Fastqsanger.gz | |||
| SRR18645015_2.fastq.gz | Fastqsanger.gz | |||
| SRR18645016_1.fastq.gz | Fastqsanger.gz |
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Project description:We hypothesised that induction of a torpor-like state would confer a radioprotective effect given the evidence that hibernation extends survival times in irradiated squirrels compared to active controls. To test this hypothesis, a torpor-like state was induced in zebrafish using melatonin treatment and cold temperatures, and radiation exposure was administered twice over the course of 10 days. The protective effects of induced-torpor were assessed via RNA sequencing of mRNA extracted from the liver. A systems-level analysis was performed on the transcriptomic data to characterise the cellular phenotypes in radiation (28.5-rad), temperature+melatonin (18.5-mel), temperature+radiation (18.5-rad), and temperature+melatonin+radiation (18.5-mel-rad) groups compared with a control group (28.5-Ctrl). The results revealed that the torpor group experiences a reduction in metabolic genes, and increased pro-survival, antiapoptotic and DNA repair genes. The radiation group had changes to lipid metabolism and absorptions, a wound healing response and an immune response. While the induced torpor group showed a response to stress including changes to metabolism and perturbation of the circadian rhythm, it also maintained the pro-survival, anti-apoptotic and DNA repair genes seen in the torpor group suggesting a conferred radio-protective effect.
2023-01-25 | GSE200212 | GEO
Project description:We hypothesised that induction of a torpor-like state would confer a radioprotective effect given the evidence that hibernation extends survival times in irradiated squirrels compared to active controls. To test this hypothesis, a torpor-like state was induced in zebrafish using melatonin treatment and cold temperature, and radiation exposure was administered twice over the course of 10 days. The protective effects of induced-torpor were assessed via RNA sequencing of mRNA extracted from the GIT. A systems level analysis was performed on the transcriptomic data to characterise the cellular phenotypes in radiation, torpor, and torpor+radiation groups. The results revealed that melatonin and cold temperature successfully induced a torpor-like state in zebrafish as shown by decreased metabolism and activity levels. Low dose radiation caused DNA damage and oxidative stress triggering a stress response, including steroidal signalling and changes to metabolism, damage to the central nervous system and cell cycle arrest. This stress response was attenuated in the torpor+radiation group by an increase in biosynthesis, proliferation, cell survival signals and expression of genes involved in protection against the adverse effects of radiation, particularly in neurons, suggesting a radioprotective effect conferred by a torpor state. This proof-of-concept model provides compelling initial evidence for utilizing an induced torpor-like state as a potential countermeasure for radiation exposure.
2021-04-28 | GSE169522 | GEO
Project description:Induced torpor as a countermeasure for low dose radiation exposure in a zebrafish model
| PRJNA716978 | ENA
Project description:Low-dose radiation refers to exposure to ionizing radiation at levels that are generally considered safe and not expected to cause immediate health effects. However, the effects of low-dose radiation are still not fully understood and research in this area is ongoing. In this study, we investigated changes in gene expression in diabetic human aortic endothelial cells (T2D-HAECs) derived from type 2 diabetes patients. To this end, we used RNA-seq to profile the transcriptomes of cells exposed to varying doses of low-dose radiation (0.1Gy, 0.5Gy, and 2.0Gy) and compared them to a control group with no radiation exposure. Differentially expressed genes and enriched pathways were identified using the DESeq2 and gene set enrichment analysis (GSEA) methods, respectively. The data generated in this study are publicly available through the gene expression omnibus (GEO) database. This study provides a valuable resource for studying the effects of low-dose radiation on T2D-HAECs and can contribute to a better understanding of the potential human health risks associated with low-dose radiation exposure.
2023-04-07 | GSE228572 | GEO
Project description:Many neural progenitor cells present in the fetus, but also in adult brain, which play a major role for the reproduction for healingin regeneration of neuronal cells, when differentiated cells are damaged. However, effects of radiation effect on undifferentiated neural progenitor cells remained unclear. The radiation doses of medical exposure, pollution by nuclear power plant accidents, and other exposure of workers; medical workers, airline crews, and astronaut have been focused. In this study, we report the effects of low- to middle- dose doses of radiation on cultured human neural progenitor cells (hNPC) differentiated derived from embryonic stem (ES) cells, which are partially compared with those of human umbilical vein endothelial cell (HUVEC). Gene expression was changed by continuous exposure of 31mGy; 0.0072 mGy/ minute, 124mGy; 0.029 mGy/ minute and 496mGy; 0.085 mGy/ minute for seventy-two hours. While shortening in neurite length by 124mGy was not significant, its decrease was observed by 496 mGy of radiation. Number of altered pathways increased dose-dependently. By thirty-one mGy per 72 hours of radiation, gene expression of inflammatory pathways involving interferon and cell junction were changed. By 124 mGy of radiation, DNA double strand break repair pathways and cell adhesion molecules were affected. Then, 496 mGy of radiation for 72 hours altered translational DNA synthesis pathway, apoptotic pathway, various metabolic pathways and neural differentiation pathways. Dose-dependent transcriptional changes by low- to middle- radiation are consistent with gradual axonal shortening, growth arrest and neural cell death.
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Project description:One of the most likely risks astronauts on long duration space missions face is exposure to ionizing radiation associated with highly energetic and charged heavy (HZE) particles. Since access to medical expertise on such a mission is limited at best, early diagnosis and mitigation of such exposure is critical. In order to accurately determine the time since exposure and dosage of exposure, dose- and time-dependent “biomarkers” are needed. Therefore, we performed a dose- and time-course transcriptional analysis for radiation exposure at 0, 0.15, 0.30, and 1.5 Gy with corresponding time points at 1 hour (hr) post-exposure as well as 2 hr and 6 hr using Affymetrix® Human PrimeArrayTM chips. The analysis of our data suggests a set of sensitive genetic biomarkers specific to each radiation level as well as generic radiation response biomarkers. Upregulated biomarkers can then be used within lab-on-a-chip (LOC) systems to detect exposure to ionizing radiation.
2017-12-01 | GSE63952 | GEO
Project description:Many neural progenitor cells present in the fetus, but also in adult brain, which play a major role for the reproduction for healingin regeneration of neuronal cells, when differentiated cells are damaged. However, effects of radiation effect on undifferentiated neural progenitor cells remained unclear. The radiation doses of medical exposure, pollution by nuclear power plant accidents, and other exposure of workers; medical workers, airline crews, and astronaut have been focused. In this study, we report the effects of low- to middle- dose doses of radiation on cultured human neural progenitor cells (hNPC) differentiated derived from embryonic stem (ES) cells, which are partially compared with those of human umbilical vein endothelial cell (HUVEC). Gene expression was changed by continuous exposure of 31mGy; 0.0072 mGy/ minute, 124mGy; 0.029 mGy/ minute and 496mGy; 0.085 mGy/ minute for seventy-two hours. While shortening in neurite length by 124mGy was not significant, its decrease was observed by 496 mGy of radiation. Number of altered pathways increased dose-dependently. By thirty-one mGy per 72 hours of radiation, gene expression of inflammatory pathways involving interferon and cell junction were changed. By 124 mGy of radiation, DNA double strand break repair pathways and cell adhesion molecules were affected. Then, 496 mGy of radiation for 72 hours altered translational DNA synthesis pathway, apoptotic pathway, various metabolic pathways and neural differentiation pathways. Dose-dependent transcriptional changes by low- to middle- radiation are consistent with gradual axonal shortening, growth arrest and neural cell death. Undifferentiated hNPC derived from embryonic stem (ES) cells and HUVECs synchronized in G1 cell cycle phase were irradiated from sealed cesium-137 for 72 h.
2015-03-31 | E-GEOD-67309 | biostudies-arrayexpress
Project description:Single-cell sequencing was performed on the irradiated cell lines to accurately map the biological information triggered by low-dose radiation to each individual cell.
2024-05-29 | GSE255800 | GEO
Project description:It is widely believed that the carcinogenic action of ionizing radiation is due to targeted DNA damage and resulting mutations, but there is also substantial evidence that non-targeted radiation effects alter epithelial phenotype and the stromal microenvironment. Activation of transforming growth factor β1 (TGFβ) is a non-targeted radiation effect that mediates cell fate decisions following DNA damage and regulates microenvironment composition; it could either suppress or promote cancer. We asked if such non-targeted radiation effects contribute to carcinogenesis by using a novel radiation chimera model. Unirradiated Trp53 null mammary epithelium was transplanted to the mammary stroma, previously divested of endogenous epithelia, of mice previously exposed to a single low (10 -100 cGy) radiation dose. By 300 days, 100% of transplants in irradiated hosts at either 10 or 100 cGy had developed Trp53 null breast carcinomas compared to 54% in unirradiated hosts. Tumor growth rate was also increased by high, but not low, dose host irradiation. In contrast, irradiation of Tgfb1 heterozygote mice prior to transplantation failed to decrease tumor latency, or increase growth rate at any dose. Host irradiation significantly reduced the latency of invasive ductal carcinoma compared to spindle cell carcinoma. However, irradiation of either host genotype significantly increased the frequency of estrogen receptor negative tumors. These data demonstrate two concepts critical to understanding radiation risks. First, non-targeted radiation effects can significantly promote the frequency and alter the features of epithelial cancer. Second, radiation-induced TGFβ activity is a key mechanism of tumor promotion. Keywords: Differential gene expression after low dose irradiation
2010-03-01 | GSE18216 | GEO
Project description:<p>Long-term low-dose ionizing radiation (LLIR) widely exists in human life and has been confirmed to have potential pathogenic effects on cancer and cardiovascular diseases. However, it is technically and ethically unfeasible to explore LLIR-induced phenotypic changes in the human cohort, leading to slow progress in revealing the pathogenesis of LLIR. In this work, we recruited 32 radiation workers and 18 healthy non-radiation workers from the same city with the same eating habits for radiation damage evaluation and metabolomics profiling. It was found that clear metabolic phenotypic differences existed between LLIR and non-LLIR exposed participants. Moreover, LLIR exposed workers can be further divided into 2 types of metabolic phenotypes, corresponding to high and low damage types, respectively. 3-hydroxypropanoate and glycolaldehyde were identified as sensitive indicators to radiation damage, which specific response to the chromosomal aberration of workers and may be potential monitoring markers for LLIR protection. Taurine metabolism-related pathways were identified as the main differential metabolic pathway under LLIR inducing, which had been confirmed to have a response to acute or chronic radiation exposure. We expect our study can be helpful to LLIR damage monitoring and symptomatic intervention in the future.</p>
2022-04-07 | MTBLS3854 | MetaboLights