Identification of DNA methylation biomarkers for evaluating cardiovascular disease risk from epigenome profiles altered by low-dose ionizing radiation
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE246076 | GEO | 2025/10/23
REPOSITORIES: GEO
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Project description:BackgroundEnvironmental exposure, medical diagnostic and therapeutic applications, and industrial utilization of radionuclides have prompted a growing focus on the risks associated with low-dose radiation (< 100 mGy). Current evidence suggests that such radiation can induce epigenetic changes. Nevertheless, whether exposure to low-dose radiation can disrupt endothelial cell function at the molecular level is unclear. Because endothelial cells play crucial roles in cardiovascular health and disease, we aimed to investigate whether low-dose radiation could lead to differential DNA methylation patterns at the genomic level in endothelial cell (EC) lines.MethodsWe screened for changes in DNA methylation patterns in primary human aortic (HAECs) and coronary artery endothelial cells following exposure to low-dose ionizing radiation. Using a subset of genes altered via DNA methylation by low-dose irradiation, we performed gene ontology (GO) analysis to predict the possible biological network mediating the effect of low-dose radiation. In addition, we performed comprehensive validation using methylation and gene expression analyses, and ChIP assay to identify useful biomarkers among candidate genes for use in detecting low-dose radiation exposure in human primary normal ECs.ResultsLow-dose radiation is sufficient to induce global DNA methylation alterations in normal EC lines. GO analysis demonstrated that these hyper- or hypo-methylated genes were linked to diverse biological pathways. Our findings indicated a robust correlation between promoter hypermethylation and transcriptional downregulation of four genes (PGRMC1, UNC119B, RERE, and FNDC3B) in response to low-dose ionizing radiation in HAECs.ConclusionsBased on these findings, the identified genes can serve as potential DNA methylation biomarkers for the assessment of cardiovascular risk upon exposure to low-dose radiation.
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Project description:Identification of DNA methylation biomarkers for evaluating cardiovascular disease risk from epigenome profiles altered by low-dose ionizing radiation
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Project description:Male mice 10-14 weeks of age were exposed in vivo to 10 rad X-ray. The objective is to extract information on gene networks from the microarray data. Keywords: Ionizing radiation
2006-10-01 | GSE4880 | GEO
Project description:Radiation therapy (RT) remains a vital component of the curative multimodality therapy for many types of cancer including breast cancer (BC). Even if great number of BC patients receive RT, not all of them report benefits, due to radioresistance activation depending also by hormone receptor status. We analyze and compare molecular responses, in term of gene expression profile (GEP) changes, induced by high dose of Ionizing Radiation (IR), in MDA-MB-231 with ER-/PR-HER2- receptor status. Moreover, we selected a MDA-MB-231 Radioresistent Cell Fraction (RCF), in which we highlighted specific molecules able to drive radioresistance. We trust that this study could have a role in the evaluating of RT response in term of radioresistance process activation to define a personalized biological-driven treatment plan in triple negative BC.
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Project description:Previous epidemiologic data demonstrate that cardiovascular (CV) morbidity and mortality may occur decades after ionizing radiation exposure. With increased use of proton and carbon ion radiotherapy and concerns about space radiation exposures to astronauts on future long-duration exploration-type missions, the long-term effects and risks of low-dose charged particle irradiation on the CV system must be better appreciated. Here we report on the long-term effects of whole-body proton ((1)H; 0.5 Gy, 1 GeV) and iron ion ((56)Fe; 0.15 Gy, 1GeV/nucleon) irradiation with and without an acute myocardial ischemia (AMI) event in mice. We show that cardiac function of proton-irradiated mice initially improves at 1 month but declines by 10 months post-irradiation. In AMI-induced mice, prior proton irradiation improved cardiac function restoration and enhanced cardiac remodeling. This was associated with increased pro-survival gene expression in cardiac tissues. In contrast, cardiac function was significantly declined in (56)Fe ion-irradiated mice at 1 and 3 months but recovered at 10 months. In addition, (56)Fe ion-irradiation led to poorer cardiac function and more adverse remodeling in AMI-induced mice, and was associated with decreased angiogenesis and pro-survival factors in cardiac tissues at any time point examined up to 10 months. This is the first study reporting CV effects following low dose proton and iron ion irradiation during normal aging and post-AMI. Understanding the biological effects of charged particle radiation qualities on the CV system is necessary both for the mitigation of space exploration CV risks and for understanding of long-term CV effects following charged particle radiotherapy.
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Project description:Long noncoding RNAs (lncRNAs) are emerging as key regulators of diverse cell functions and processes. However, the relevance of lncRNAs in the cell and tissue response to ionizing radiation has not yet been characterized. Here we used microarray profiling to determine lncRNA and mRNA expression in mammary glands of BALB/c and SPRET/EiJ mice after low-dose ionizing radiation (LDIR) exposure. We found that unirradiated mammary tissues of these strains differed significantly in baseline expressions of 290 lncRNAs. LDIR exposure (10 cGy) induced a significant change in the expression of many lncRNAs. For BALB/c mice, a total of 357, 480, and 335 lncRNAs and 550, 911, and 389 coding RNAs were identified at 2, 4, and 8 weeks post-irradiation, respectively, while for SPRET/EiJ, a total of 327 lncRNAs and 424 mRNAs were identified at 4 weeks post-irradiation.
2014-12-01 | GSE62662 | GEO
Project description:The ability to detect trace amounts of ionizing radiation is a paramount concern for chemical, biological, radiological, nuclear, and explosives (CBRNE) operations and observation of clandestine activities in the event of source relocation and contamination. Microbes respond to environmental stress such as fluctuations in pH and temperature, nutrient limited conditions, and oxidative stress with morphological and behavioral changes, and induced responses are known to persist after the stressor is removed. Innate responses to other external stressors like exposure to low-dose ionizing radiation could be measured and characterized by changes in gene expression and resulting transcriptional changes could by engineered into biosensors to monitor and discern the presence and type of radiation, respectively, in the environment. The current understanding of the biological and transcriptional responses of bacteria to various doses of ionizing radiation is minimal. The work in this study expands upon the findings in our previous study of the response of a model bacterium to low doses of ionizing radiation soil bacterium, Pseudomonas putida KT2440. Following exposure to an approximate absorbed dose rate of 9 mGy d-1 of a 239Pu, 3H, or 55Fe source, RNA-seq analysis revealed key changes in gene expression of P. putida of genes encoding membrane components, central carbon metabolism, DNA repair pathways, and motility. Several genes were differentially expressed genes in P. putida after exposure to multiple radionuclide sources. Moreover, other genes were uniquely differentially expressed by a single radionuclide source. These findings expand upon the limited understanding of the biological response to low doses of ionizing radiation and provide fundamental characterization required to develop discriminatory RNA-based biosensors.
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Project description:In the context of radiotherapy, the effects elicited by ionizing radiation on the supportive stroma of tumors remains understudied. Tumor infiltrating fibroblasts are abundantly found in the stromal tissue of most tumor types and are key determinants of tumor progression and metastasis. Given the clinical attention that ablative radiotherapy is gaining nowadays, and the paramount role played by CAFs in cancer sustainability, in this study the effect of high-dose ionizing radiation on primary CAF?S have been investigated. We have used high-throughput transcriptome analysis to ascertain in which degree tumor stromal fibroblast become pro-tumorigenic or anti-tumorigenic after ablative irradiation. Hence, genome-wide transcriptome analysis has been carried out on CAFs isolated from NSCLC tumors after receiving a single dose of 18 Gray. The expressions of relevant genes have been validated by real-time PCR, and transformed cellular pathways have been checked by functional assays. Overall, our data reveals profound changes in biological pathways including cellular stress, DNA damage, cell cycle, aging, apoptosis, oxidative stress, and matrix remodeling. Ablative radiation doses may exert both pro-and anti-tumorigenic effects on CAFs. The ultimate effect of such disturbances merits further investigation in more complex in vivo settings.
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Project description:Effect of low dose ionizing radiation on gene expression profile in human lymphocytes.
2013-05-11 | E-MEXP-2918 | biostudies-arrayexpress
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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