Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA307094 | ENA |
REPOSITORIES: ENA
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Project description:Low and high doses of X-rays are used in medicine as diagnostic and therapeutic tools, respectively. While response to high doses of radiation is well known, contradictions exist about effects of low-dose irradiation. Therefore, improving the knowledge on the consequences of low-dose irradiation could help to address this controversy. Moreover, describing new insights into high-dose irradiation would improve new cancer therapies combining radiation and gene therapy. As long non-coding RNAs (lncRNAs) seems to be engaged to almost all biological functions, including response to DNA damage, we aimed to describe the participation of lncRNAs in the response to different doses of X-ray exposure. We observed that, in human breast epithelial cells, different sets of coding and non-coding transcripts are differentially regulated at moderate and high doses compared to low doses. The validation of expression of five lncRNAs only regulated at high and moderate X-ray doses supports our results. Altogether, we could conclude that response to moderate and high dose irradiation versus response to low-doses also differs in terms of lncRNA expression. Therefore, further studies on the participation of lncRNAs in this response to radiation would help to address controversies regarding low-dose irradiation response and to improve therapies using high-dose irradiation.
2016-08-31 | GSE76357 | GEO
Project description:Biological tissues are exposed to X-rays under controlled conditions in both medical applications (diagnostic imaging and radiotherapy) and research studies (e.g. microcomputed X-ray tomography: microCT). Radiotherapy regimes may deliver doses of up to 50Gy to both the target tumour and to healthy tissues resulting in undesirable clinical side effects which can severely compromise quality of life. The substantially higher doses used in microCT imaging (in the kGy range) may, in the case of native (non-fixed tissues), impact on structure and hence function. Whilst the interaction between X-rays and cells is relatively well-characterised, X-ray-induced structural damage to the extracellular matrix (ECM) is poorly understood. In this study, we test the hypothesis that ECM proteins and ECM-rich tissues (purified collagen I and tendons) are structurally and functionally compromised by exposure to X-rays doses ranging from 50Gy (breast radiotherapy) to 495kGY (synchrotron imaging). Using protein gel electrophoresis we show that breast radiotherapy equivalent doses affect the constituent α chains of solubilised purified collagen I whilst assembly into fibrils, either in vitro or in vivo, prevents X-ray-induced fragmentation but not structural damage (as characterised by LC-MS/MS and peptide location fingerprinting: PLF). In the case of synchrotron imaging, the resultant X-ray exposure induces substantial fragmentation of both constituent collagen I α chains and the triple-helical monomer. Mass spectrometry and PLF analysis of synchrotron irradiated tendon identified structure-associated changes in collagens I, VI, XII, the large proteoglycan aggrecan, small leucine-rich proteoglycans decorin and fibromodulin and a key elastic fibre component fibulin-1. Synchrotron imaging also compromises the mechanical behaviour of tendons. We conclude, therefore, that exposure to both radiotherapy and synchrotron imaging X-rays can profoundly affect the structure of key tissue ECM components with implications for tissue function, downstream cell-matrix interactions, and the interpretation of in situ mechanical data.
2025-03-11 | PXD050691 | Pride
Project description:Biological tissues are exposed to X-rays under controlled conditions in both medical applications (diagnostic imaging and radiotherapy) and research studies (e.g. microcomputed X-ray tomography: microCT). Radiotherapy regimes may deliver doses of up to 50Gy to both the target tumour and to healthy tissues resulting in undesirable clinical side effects which can severely compromise quality of life. The substantially higher doses used in microCT imaging (in the kGy range) may, in the case of native (non-fixed tissues), impact on structure and hence function. Whilst the interaction between X-rays and cells is relatively well-characterised, X-ray-induced structural damage to the extracellular matrix (ECM) is poorly understood. In this study, we test the hypothesis that ECM proteins and ECM-rich tissues (purified collagen I and tendons) are structurally and functionally compromised by exposure to X-rays doses ranging from 50Gy (breast radiotherapy) to 495kGY (synchrotron imaging). Using protein gel electrophoresis we show that breast radiotherapy equivalent doses affect the constituent α chains of solubilised purified collagen I whilst assembly into fibrils, either in vitro or in vivo, prevents X-ray-induced fragmentation but not structural damage (as characterised by LC-MS/MS and peptide location fingerprinting: PLF). In the case of synchrotron imaging, the resultant X-ray exposure induces substantial fragmentation of both constituent collagen I α chains and the triple-helical monomer. Mass spectrometry and PLF analysis of synchrotron irradiated tendon identified structure-associated changes in collagens I, VI, XII, the large proteoglycan aggrecan, small leucine-rich proteoglycans decorin and fibromodulin and a key elastic fibre component fibulin-1. Synchrotron imaging also compromises the mechanical behaviour of tendons. We conclude, therefore, that exposure to both radiotherapy and synchrotron imaging X-rays can profoundly affect the structure of key tissue ECM components with implications for tissue function, downstream cell-matrix interactions, and the interpretation of in situ mechanical data.
2025-03-11 | PXD050686 | Pride
Project description:Biological tissues are exposed to X-rays under controlled conditions in both medical applications (diagnostic imaging and radiotherapy) and research studies (e.g. microcomputed X-ray tomography: microCT). Radiotherapy regimes may deliver doses of up to 50Gy to both the target tumour and to healthy tissues resulting in undesirable clinical side effects which can severely compromise quality of life. The substantially higher doses used in microCT imaging (in the kGy range) may, in the case of native (non-fixed tissues), impact on structure and hence function. Whilst the interaction between X-rays and cells is relatively well-characterised, X-ray-induced structural damage to the extracellular matrix (ECM) is poorly understood. In this study, we test the hypothesis that ECM proteins and ECM-rich tissues (purified collagen I and tendons) are structurally and functionally compromised by exposure to X-rays doses ranging from 50Gy (breast radiotherapy) to 495kGY (synchrotron imaging). Using protein gel electrophoresis we show that breast radiotherapy equivalent doses affect the constituent α chains of solubilised purified collagen I whilst assembly into fibrils, either in vitro or in vivo, prevents X-ray-induced fragmentation but not structural damage (as characterised by LC-MS/MS and peptide location fingerprinting: PLF). In the case of synchrotron imaging, the resultant X-ray exposure induces substantial fragmentation of both constituent collagen I α chains and the triple-helical monomer. Mass spectrometry and PLF analysis of synchrotron irradiated tendon identified structure-associated changes in collagens I, VI, XII, the large proteoglycan aggrecan, small leucine-rich proteoglycans decorin and fibromodulin and a key elastic fibre component fibulin-1. Synchrotron imaging also compromises the mechanical behaviour of tendons. We conclude, therefore, that exposure to both radiotherapy and synchrotron imaging X-rays can profoundly affect the structure of key tissue ECM components with implications for tissue function, downstream cell-matrix interactions, and the interpretation of in situ mechanical data.
2025-03-11 | PXD050689 | Pride
Project description:Biological tissues are exposed to X-rays under controlled conditions in both medical applications (diagnostic imaging and radiotherapy) and research studies (e.g. microcomputed X-ray tomography: microCT). Radiotherapy regimes may deliver doses of up to 50Gy to both the target tumour and to healthy tissues resulting in undesirable clinical side effects which can severely compromise quality of life. The substantially higher doses used in microCT imaging (in the kGy range) may, in the case of native (non-fixed tissues), impact on structure and hence function. Whilst the interaction between X-rays and cells is relatively well-characterised, X-ray-induced structural damage to the extracellular matrix (ECM) is poorly understood. In this study, we test the hypothesis that ECM proteins and ECM-rich tissues (purified collagen I and tendons) are structurally and functionally compromised by exposure to X-rays doses ranging from 50Gy (breast radiotherapy) to 495kGY (synchrotron imaging). Using protein gel electrophoresis we show that breast radiotherapy equivalent doses affect the constituent α chains of solubilised purified collagen I whilst assembly into fibrils, either in vitro or in vivo, prevents X-ray-induced fragmentation but not structural damage (as characterised by LC-MS/MS and peptide location fingerprinting: PLF). In the case of synchrotron imaging, the resultant X-ray exposure induces substantial fragmentation of both constituent collagen I α chains and the triple-helical monomer. Mass spectrometry and PLF analysis of synchrotron irradiated tendon identified structure-associated changes in collagens I, VI, XII, the large proteoglycan aggrecan, small leucine-rich proteoglycans decorin and fibromodulin and a key elastic fibre component fibulin-1. Synchrotron imaging also compromises the mechanical behaviour of tendons. We conclude, therefore, that exposure to both radiotherapy and synchrotron imaging X-rays can profoundly affect the structure of key tissue ECM components with implications for tissue function, downstream cell-matrix interactions, and the interpretation of in situ mechanical data.
2025-03-11 | PXD050690 | Pride
Project description:MicroRNA (miRNA) is a type of non-coding RNA that regulates the expression of its target genes by interacting with the complementary sequence of the target mRNA molecules. Recent evidence has shown that genotoxic stress induces miRNA expression, but the target genes involved and role in cellular responses remain unclear. We examined the role of miRNA in the cellular response to X-ray irradiation by studying the expression profiles of radio-responsive miRNAs and their target genes in cultured human cell lines. We found that expression of miR-574-3p was induced in the lung cancer cell line A549 by X-ray irradiation. Overexpression of miR-574-3p caused delayed growth in A549 cells. A predicted target site was detected in the 3'-untranslated region of the enhancer of the rudimentary homolog (ERH) gene, and transfected cells showed an interaction between the luciferase reporter containing the target sequences and miR-574-3p. Overexpression of miR-574-3p suppressed ERH protein production and delayed cell growth. This delay was confirmed by knockdown of ERH expression. Our study suggests that miR-574-3p may contribute to the regulation of the cell cycle in response to X-ray irradiation via suppression of ERH protein production. miRNA expression were measured at 1 and 3 h after exposure to doses of 0, 2 or 20 Gy. Microarray experiments were performed with duplicate for each experiment.
2014-03-14 | E-GEOD-30130 | biostudies-arrayexpress
Project description:This dataset is composed by the transcriptomic, proteomic and phosphoproteomic profile of primary human fibroblasts exposed to two different doses of radiation: an acute X-ray radiation dose, and an accumulative X-ray radiation dose. These data were employed to apply and evaluate different computational approaches to model and infer cellular signaling processes through the combination of prior knowledge and omic data. We employed RNA-Seq and Mass Spectrometry (MS) to generate the transcriptomic and proteomic data from the RNA and protein samples, respectively.
2023-01-01 | E-MTAB-10456 | biostudies-arrayexpress
Project description:Early exposure to xenoestrogens may predispose to breat cancer risk later in adult life. The long-lived, self-regenerating epithelial progenitor cells are more susceptible to these exposure injuries and transmit the injured memory throught epigenetic mechanisms to their differentiated progeny. We have established a breast progenitor model for epigenetic study and our previous work demonstrated that DNA methylation profiling of epithelial progeny derived from progenitors exposed to estradiol detected hypermethylated loci in 0.5% of protein-coding genes. In this study, we extended this exposure study to non-coding microRNA genes.
2012-04-16 | GSE16001 | GEO
Project description:Early exposure to xenoestrogens may predispose to breat cancer risk later in adult life. The long-lived, self-regenerating epithelial progenitor cells are more susceptible to these exposure injuries and transmit the injured memory throught epigenetic mechanisms to their differentiated progeny. We have established a breast progenitor model for epigenetic study and our previous work demonstrated that DNA methylation profiling of epithelial progeny derived from progenitors exposed to estradiol detected hypermethylated loci in 0.5% of protein-coding genes. In this study, we extended this exposure study to non-coding microRNA genes. Three mammosphere-derived epithelial cell (MDEC) sample sets from three independent patients. Each sample set includes one DES-preexposed and one DMSO-preexposed MDEC.
2012-04-15 | E-GEOD-16001 | biostudies-arrayexpress
Project description:Exposure to radiation provokes cellular responses controlled in part by gene expression networks. MicroRNAs (miRNAs) are small non-coding RNAs which mostly regulate gene expression by degrading the messages or inhibiting translation. Here, we investigated changes in miRNA expression patterns after low (0.1 Gy) and high (2.0 Gy) doses of X-ray in human fibroblasts. At early (0.5 h) and late (6 and 24 h) time points, irradiation caused qualitative and quantitative differences in the down-regulation of miRNA levels, including miR-92b, 137, 660, and 656. A transient up-regulation of miRNAs was observed after 2 h post-irradiation following high doses of radiation, including miR-558 and 662. MicroRNA levels were inversely correlated with targets from mRNA and proteomic profiling after 2.0 Gy of radiation. MicroRNAs miR-579, 608, 548-3p, and 585 are noted for targeting genes involved in radioresponsive mechanisms, such as cell cycle checkpoint and apoptosis. We suggest here a model in which miRNAs may act as "hub" regulators of specific cellular responses, immediately down-regulated so as to stimulate DNA repair mechanisms, followed by up-regulation involved in suppressing apoptosis for cell survival. Taken together, miRNAs may mediate signaling pathways in sequential fashion in response to radiation, and may serve as biodosimetric markers of radiation exposure. The gene expression patterns in human fibroblasts after 2.0 Gy of low-LET radiation was determined at 2 and 24 hrs post-irradiation time in technical triplicates. Control non-irradiated samples were also prepared in triplicates.
2010-06-20 | E-GEOD-12647 | biostudies-arrayexpress