Single-cell RNA-Seq of blood cells between an irradiated patient and non-irradiated healthy men
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE166902 | GEO | 2021/08/11
REPOSITORIES: GEO
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Project description:In order to identified as candidate biomarkers for early diagonosis or as therapeutic targets in late damages of ionizing radiation, gene expression profile was analyzed in the peripheral blood of three 60Co γ-ray accidently-exposed persons. The results showed that there were 285 up-regulated and 446 down-regulated genes in irradiated samples compared with control samples. The large majority of those differentially expressed genes encode proteins that are associated with immune response, inflammation, cell structure, oxidative stress, neuro-hormone regulation, reproduction, susceptibility of psychiatric disorders, and transcriptional regulators. The expressions of IL3, KDR, CEACAM8 and OSM were validated by real-time RT-PCR method. The findings of our study should help us understanding the molecular mechanisms underlying the late effects of ionizing radiation and to develop better diagonostic and therapeutic strategies for those damages. Fresh blood samples were collected from three 60Coγ-Ray accidentally-exposed persons(3 years post irradiation) and three non-irradiated healthy donors. Leucocytes cells were isolated and total RNA was extracted. Four RNA samples, from three accidently-exposed persons and a RNA mixture extracted from a combination of three healthy donors` leucocytes (ratio 1:1:1, each 3.3×106 cells) in EL buffer, were subjected to Agilent gene expression microarray assay.
2012-11-01 | E-GEOD-34131 | biostudies-arrayexpress
Project description:Single-cell RNA-Seq of blood cells between an irradiated patient and non-irradiated healthy men
| PRJNA702194 | ENA
Project description:In order to identified as candidate biomarkers for early diagonosis or as therapeutic targets in late damages of ionizing radiation, gene expression profile was analyzed in the peripheral blood of three 60Co γ-ray accidently-exposed persons. The results showed that there were 285 up-regulated and 446 down-regulated genes in irradiated samples compared with control samples. The large majority of those differentially expressed genes encode proteins that are associated with immune response, inflammation, cell structure, oxidative stress, neuro-hormone regulation, reproduction, susceptibility of psychiatric disorders, and transcriptional regulators. The expressions of IL3, KDR, CEACAM8 and OSM were validated by real-time RT-PCR method. The findings of our study should help us understanding the molecular mechanisms underlying the late effects of ionizing radiation and to develop better diagonostic and therapeutic strategies for those damages.
2012-11-01 | GSE34131 | GEO
Project description:CEA_SGF:E00006# This set of experiments was performed in order to identify radiation responsive genes. For this, differentiated cultures derived from a single donor were irradiated at either 1 cGy, 2 Gy or sham-irradiated at T0 and total RNA extracts were prepared at 6 time points post-irradiation. Irradiated samples for each dose were hybridized seperately with sham-irradiated samples at the same time point. Each time point for each individual dose was assessed with two independent dye-swap hybridizations. Keywords: time-course
2004-11-01 | GSE1370 | GEO
Project description:The vascular endothelium is a hot spot in the response to radiation therapy for both tumors and normal tissues. To improve patient outcomes, interpretable systemic hypotheses are needed to help radiobiologists and radiation oncologists propose endothelial targets that could protect normal tissues from the adverse effects of radiation therapy and/or enhance its antitumor potential. To this end, we captured the kinetics of multi-omics layers – i.e. miRNome, targeted transcriptome, proteome and metabolome – in irradiated primary human endothelial cells cultured in vitro. We then designed a strategy of deep learning as in convolutional graph networks that facilitates unsupervised high-level feature extraction of important omics data to learn how ionizing radiation-induced endothelial dysfunction may evolve over time. Last, we present experimental data showing that some of the features identified using our approach are involved in the alteration of angiogenesis by ionizing radiation.
2022-01-19 | PXD030572 | Pride
Project description:This study aims to compare mRNA expression between irradiated and non-irradiated keloid-derived primary cells by RNA-Seq. In this study, keloid-derived primary cells that were isolated from patients, and then divided into three groups and each group had four repeats. The first group of cells was treated without radiation, the second group of cells were received 4 Gy delivered in 2-Gy fractions once per day over 2 days and the third group of cells were received 8 Gy delivered in 2-Gy fractions once per day over 4 days.The last two groups of cells were irradiated at a fixed rate of 1.15 Gy/min using an X-ray linear accelerator (Rad Source Technologies Inc., Suwanee, GA, USA). 24 hours post irradiation of the third group of cells, all keloid-derived primary cells were collected and subjected to mRNA expression analysis.
2020-07-11 | GSE154234 | GEO
Project description:In this project, we aimed to examine the transcriptional changes that occur after irradiation of intestinal organoid-derived subcutaneous heterotopic tumors over a 7 day period post-radiation treatment. AKPT (villinCreER;Apcfl/fl;KrasG12D/+;Trp53fl/fl;TgfbrIfl/fl) intestinal organoids were cultured, then suspended in a 50:50 phosphate buffered-saline and Matrigel mixture and subcutaneously implanted into male C57BL/6 mice. Two weeks after implantation, mice were given either a single dose of 15 Gy radiation or 3 doses of 7 Gy radiation. Tumours were harvested 4 hours, 24 hours, 3 days, and 7 days after receiving the single dose of 15 Gy or the final dose of 7 Gy radiation, as well as from corresponding non-irradiated controls. RNA was extracted from the collected tumours and processed for RNA sequencing.
2023-01-25 | E-MTAB-12538 | biostudies-arrayexpress
Project description:Background: The brain undergoes ionizing radiation exposure in many clinical situations, particularly during radiotherapy for brain tumors. The critical role of hippocampus in the pathogenesis of radiation-induced neurocognitive dysfunction is well recognized. Aim: The goal of this study is to test the potential contribution of non-targeted effects in the detrimental response of hippocampus to irradiation and to elucidate the mechanisms involved. Material and Methods: C57Bl/6 mice were whole body (WBI) or partial body (PBI) irradiated with 0.1 or 2.0 Gy of X-rays or sham irradiated. PBI consisted in the exposure of the lower third of the mouse body, whilst the upper two thirds were shielded. Hippocampi were collected 15 days or 6 months post-irradiation and a multi-omics approach was adopted to assess the molecular changes in non-coding RNAs, proteins and metabolic levels, as well as histological changes in the rate of hippocampal neurogenesis. Results: Notably, at 2.0 Gy the pattern of early molecular and histopathological changes induced in the hippocampus at 15 days following PBI was similar in quality and quantity to the effects induced by WBI, thus providing a proof of principle of the existence of out-of-target radiation response in the hippocampus of conventional mice. We detected major alterations in DAG/IP3 and TGF- signaling pathways as well as in the expression of proteins involved in the regulation of long-term neuronal synaptic plasticity and synapse organization, coupled with defects in NSCs self-renewal in the hippocampal dentate gyrus. However, compared to the persistence of the WBI effects, most of the PBI effects were only transient and tended to decrease at 6 months post-irradiation, indicating important mechanistic difference. On the contrary, at low dose we identified a progressive accumulation of molecular defects that tended to manifest at later post-irradiation times. These data, indicating that both targeted and non-targeted radiation effects might contribute to the pathogenesis of hippocampal radiation-damage, have general implications for human health
2021-09-10 | PXD024975 | Pride
Project description:Irradiated dying tumor cells play crucial roles in tumor repopulation. However, the transcriptome changes in pancreatic cancer cells after radiation remains unknown. Here we performed RNA-sequencing in pancreatic cancer cell line SW1990 and PANC-1 that were 10Gy irradiated or unirradiated. Bioinformatic analysis revealed that the transcriptomes were significantly changed after radiation. Gene Ontology (GO) analysis revealed that the signaling concerning extracellular vesicles, especially exosomes, were significantly enriched. Further investigation revealed the vital role of irradiated dying tumor cells-derived exosomes in potentiating tumor repopulation.
2020-06-14 | GSE138984 | GEO
Project description:Glioblastomas (GBM) are brain tumors which display a bad prognosis despite conventional treatment associating surgical resection and subsequent radio-chemotherapy. These tumors are defined by an abundant and abnormal vascularization as well as by an important cellular heterogeneity. GBM notably contain a subpopulation of GBM stem-like cells (GSC) which contribute to tumor aggressiveness, resistance, and recurrence. Moreover, GSC directly take part in the formation of new vessels via their transdifferentiation into tumor derived endothelial cells (TDEC). Considering the importance of the vascularization in the GBM, we postulate that radiation could enhance the transdifferentiation of GSC into TDEC. Here, we show that ionizing radiation potentiates endothelial features of TDEC obtained from 3 patient-derived primocultures of GSC. Indeed, TDEC obtained from irradiated GSC (TDEC IR+) migrate more towards VEGF, form more pseudotubes in Matrigel in vitro and develop more functional blood vessel in Matrigel plugs implanted in Nude mice than TDEC obtained from non-irradiated GSC. Transcriptomic analysis allows us to highlight an overexpression of Tie2 in TDEC IR+ which is associated with the activation of AKT signaling pathway. All radiation-induced effects on TDEC IR+ were abolished by using a Tie2 kinase inhibitor, confirming the role of Tie2 signaling pathway in this process. Finally, the number of Tie2+ vessels is increased in recurrent GBM compared with matched untreated tumors. In conclusion, we show that irradiation potentiates proangiogenic features of TDEC throught Tie2/AKT signaling pathway. New therapeutic stategies associating standard teatment and an inhibitor of Tie2 signaling pathway should be considered for forthcoming trials.
2019-10-02 | GSE138236 | GEO