Epigenetic regulation of gene expression in mouse skin after ionizing radiation damage
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA698225 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13587916_1.fastq.gz | Fastqsanger.gz | |||
| SRR13587916_2.fastq.gz | Fastqsanger.gz | |||
| SRR13587917_1.fastq.gz | Fastqsanger.gz | |||
| SRR13587917_2.fastq.gz | Fastqsanger.gz | |||
| SRR13587918.fastq.gz | Fastqsanger.gz |
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Project description:Back skin from 8-10 weeks male mice was plucked to induce actively growing hair follicles. After 9 days, the back skin was irradiated with 5Gy ionizing radiation. Skin samples were collected for CHIP-seq analysis using a p53 antibody and H3K4me3 antibody. We compared wild type and Krt17 knock out mice for their epigenetic regulation of gene expression change in response to ionizing radiation
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Project description:Both exposure to ionizing radiation and obesity have been associated with various pathologies including cancer. There is a crucial need in better understanding the interactions between ionizing radiation effects (especially at low doses) and other risk factors, such as obesity. In order to evaluate radiation responses in obese animals, C3H and C57BL/6 mice fed a control low fat or a high fat (HF) diet were exposed to fractionated doses of X-rays (4×0.75 Gy). Bone marrow micronucleus assays did not suggest a modulation of radiation-induced genotoxicity by HF diet. Both HF diet and irradiation resulted in increased oxidative damage, H2AX levels and proliferation in C57BL/6 mouse liver. Using methylation-specific PCR, we observed that the promoters of p16 and Dapk genes were methylated in the livers of C57BL/6 mice fed a HF diet (irradiated and non-irradiated); Mgmt promoter was methylated in irradiated and/or HF diet-fed mice. In addition, methylation PCR arrays identified Ep300 and Socs1 (whose promoters exhibited higher methylation levels in non-irradiated HF diet-fed mice) as potential targets for further studies. We then compared microRNA regulations after radiation exposure in the livers of C57BL/6 mice fed a normal or an HF diet, using microRNA arrays. Interestingly, radiation-triggered microRNA regulations observed in normal mice were not observed in obese mice. All together, our results suggested the existence of dietary effects on radiation responses (especially epigenetic regulations) in mice, possibly in relationship with obesity-induced chronic oxidative stress. C57BL/6J mice were fed a normal or a high-fat diet and exposed to 4 x 0.75 Gy X-rays. miRNA expression was measured in the livers of 3 mice for each experimental group.
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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>
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