FLASH Irradiation Modulates Immune Responses and Accelerates Lung Recovery: A Single-Cell Perspective
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1269944 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR33764422_1.fastq.gz | Fastqsanger.gz | |||
| SRR33764422_2.fastq.gz | Fastqsanger.gz | |||
| SRR33764423_1.fastq.gz | Fastqsanger.gz | |||
| SRR33764423_2.fastq.gz | Fastqsanger.gz |
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Project description:Thoracic radiation therapy is limited by the development of acute (i.e. pneumonitis) and late (i.e. pulmonary fibrosis) side-effects. The goal of this study is to analyze, at the single cell level, the molecular impact of two radiation treatments : a conventional/clinical (CONV) modality vs. FLASH, a new radiation method that spares healthy tissue from late radiation-induced toxicities (Science Translational Medicine 6: 245ra293, 2014). We analyzed by single cell RNA sequencing (scRNAseq) dissociated lung cells from a non-irradiated control mouse (NI), a mouse 4 days after CONV thoracic irradiation (CONV) and a mouse 4 days after FLASH irradiation (FLASH). We identify transcriptional alterations induced in the distinct lung cell types after irradiation and show that FLASH irradiated lung cells present a reduced pro-inflammatory phenotype as well as a diminished activation of epithelial lung progenitor cells. In line with previous report (Radiother Oncol 124: 365-9, 2017), this study indicates that FLASH radiation therapy limits inflammation and preserves the regenerative capcity of the lung.
2019-12-07 | GSE133992 | GEO
Project description:Microarray analysis was used to identify the differentially expressed genes. Bioinformatics analyses integrated with databases and text-mined gene network were conducted to understand irradiation-related hub genes, pathways and biological processes. Our hypothesis in these paper are: 1) the expression profiles of irradiation damaged bone marrow tissue are not identical in injury phase and recovery phase; and 2) some hub genes potentially vital to BM recovery can be screened out by means of microarray analysis and bioinformatics analysis. The results provide basic information to explain the radiation-related biological processes and hub genes. The five mRNA samples in total bone marrow cells were profiled by using gene chip at 3, 7, 11 and 21 days after irradiation and 0 day (sham-irradiation) as control. Each time point contains one sample.
2013-06-17 | E-GEOD-28195 | biostudies-arrayexpress
Project description:Microarray analysis was used to identify the differentially expressed genes. Bioinformatics analyses integrated with databases and text-mined gene network were conducted to understand irradiation-related hub genes, pathways and biological processes. Our hypothesis in these paper are: 1) the expression profiles of irradiation damaged bone marrow tissue are not identical in injury phase and recovery phase; and 2) some hub genes potentially vital to BM recovery can be screened out by means of microarray analysis and bioinformatics analysis. The results provide basic information to explain the radiation-related biological processes and hub genes.
2013-06-17 | GSE28195 | GEO
Project description:DNA damage causes cancer, impairs development and accelerates aging. UV irradiation induces transcription-blocking lesions and defects in transcription-coupled nucleotide excision repair lead to developmental failure and premature aging in humans. Following DNA repair, the homeostatic processes need to be reestablished to ensure development and maintain tissue functionality. Here, we report that in C. elegans removal of the MLL/COMPASS H3K4 methyltransferase exacerbates the developmental growth retardation and accelerates aging, while depletion of the H3K4 demethylase, SPR-5, promotes developmental growth and extends lifespan amid UV-induced damage. We demonstrate that specifically the DDR-induced H3K4me2 is associated with the activation of genes regulating RNA transport, splicing, ribosome biogenesis, and protein homeostasis and regulates the recovery of protein biosynthesis that is essential for survival of UV-induced DNA damage. Our study uncovers a role of H3K4me2 in coordinating the recovery of protein biosynthesis and homeostasis that is required for developmental growth and longevity after DNA damage.
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Project description:Despite numerous observations of effects of estrogens on spermatogenesis, identification of estrogen-regulated genes in the testis is limited. We previously showed in rats, in which irradiation had completely blocked spermatogonial differentiation, that testosterone (T) suppression with GnRH-antagonist and antiandrogen stimulated spermatogenic recovery and addition of estradiol (E2) to this regimen accelerated this recovery. We report here the global changes in testicular cell gene expression induced by the E2 treatment. By minimizing the changes in other hormones and also having concurrent data on the regulation of the genes by those hormones, we were able to dissect the effects of estrogen on gene expression, independent of gonadotropin or T changes. Expression of 20 genes, largely in somatic cells, was up- or down-regulated between 2- and 5-fold by E2. There were also early germ cell genes whose expression increased but this was a result of a small increase in spermatogonial numbers. The striking enrichment of transcripts not corresponding to known genes among the E2-downregulated probes led to the identification of one as micro-RNA miR-34a. We propose that genes whose expression levels are altered in one direction by irradiation and in the opposite direction by both T suppression and E2 treatment are candidates for controlling the block in differentiation. Several genes, including insulin-like 3 (Insl3), satisfied those criteria. If they are indeed involved in the inhibition of spermatogonial differentiation, they may be candidate targets for clinical treatments to enhance recovery of spermatogenesis following gonadotoxic exposures, such as those resulting from cancer therapy. 6 sample replicates of hormonal ablation plus estradiol treatment, compared to previous 14 Sample replicates of sham treatment and 11 Sample replicates of hormonal ablation treatment groups in GSE15243
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Project description:Purpose: Tumor hypoxia is a major cause of treatment resistance, especially to radiation therapy at conventional dose rate (CONV), and we wanted to assess whether hypoxia does alter tumor sensitivity to FLASH. Methods and materials: We engrafted several tumor types (glioblastoma [GBM], head and neck cancer, and lung adenocarcinoma) subcutaneously in mice to provide a reliable and rigorous way to modulate oxygen supply via vascular clamping or carbogen breathing. We irradiated tumors using a single 20-Gy fraction at either CONV or FLASH, measured oxygen tension, monitored tumor growth, and sampled tumors for bulk RNAseq and pimonidazole analysis. Next, we inhibited glycolysis with trametinib in GBM tumors to enhance FLASH efficacy. Results: Using various subcutaneous tumor models, and in contrast to CONV, FLASH retained antitumor efficacy under acute hypoxia. These findings show that in addition to normal tissue sparing, FLASH could overcome hypoxia-mediated tumor resistance. Follow-up molecular analysis using RNAseq profiling uncovered a FLASH-specific profile in human GBM that involved cell-cycle arrest, decreased ribosomal biogenesis, and a switch from oxidative phosphorylation to glycolysis. Glycolysis inhibition by trametinib enhanced FLASH efficacy in both normal and clamped conditions. Conclusions: These data provide new and specific insights showing the efficacy of FLASH in a radiation-resistant context, proving an additional benefit of FLASH over CONV.
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