Cranial irradiation in juvenile female rats induces late-onset obesity and metabolic disturbances
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ABSTRACT:
PROVIDER: PRJEB28023 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2730120.fastq.gz | Fastqsanger.gz | |||
| ERR2730111.fastq.gz | Fastqsanger.gz | |||
| ERR2730121.fastq.gz | Fastqsanger.gz | |||
| ERR2730112.fastq.gz | Fastqsanger.gz | |||
| ERR2730122.fastq.gz | Fastqsanger.gz |
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Project description:Cranial and craniospinal irradiation are the oldest central nervous system prophylaxis treatments considered for pediatric patients with lymphoblastic leukemia (ALL). However, survivors of childhood ALL that received cranial radiotherapy are at increased risk for deficits in neurocognitive skills. The continuous and dynamic response of normal tissue after irradiation has been identified as one of the causative factors for cognitive changes after cranial radiation therapy. The aim of our study was to investigate the radiation effects on social behavior and neuronal morphology in the hippocampus of adult mice. Twenty-one-day-old male C57BL/6 mice were irradiated with the small-animal radiation research platform (SARRP). Animals were given a single 10-Gy dose of radiation of X-ray cranial radiation. One month following irradiation, animals underwent behavioral testing in the Three-Chamber Sociability paradigm. Radiation affected social discrimination during the third stage eliciting an inability to discriminate between the familiar and stranger mouse, while sham successfully spent more time exploring the novel stranger. Proteomic analysis revealed dysregulation of metabolic and signaling pathways associated with neurocognitive dysfunction such as mitochondrial dysfunction, Rac 1 signaling, and synaptogenesis signaling. We observed significant decreases in mushroom spine density in the Cornu Ammonis 2 of the hippocampus, which is associated sociability processing.
2022-02-15 | PXD017596 | Pride
Project description:Cranial irradiation (IR), an effective tool to treat malignant brain tumors, triggers a chronic pro-inflammatory microglial response, at least in the adult brain. Using bulk RNA sequencing, we show that the microglial response in the juvenile mouse hippocampus is rapid, but returns toward normal within 1 week. The sensome of irradiated hippocampal microglia reveals an immediate response that declines after one day. Irradiation of the juvenile brain induces a highly ordered temporal progression of the inflammatory and phenotypic microglial genes
2020-06-02 | GSE149522 | GEO
Project description:Healthy adult male C57BL/6 mice (8 weeks of age) were randomly divided into sham irradiation group (sham) and cranial ir-radiation group (5 Gy 4 d). For the 5 Gy 4 d group, the head of mice were received 20 Gy X-rays (RAD Source RS 2000 series, Suwanee, USA), applied as four doses of 5 Gy in consecutive 4 days at a dose rate of 2.33 Gy/ min. The rest of mouse’s body was completely protected by a 2-cm thick lead shield. For the sham group, the mice were maintained in the same procedure except X-ray irradiation. No radiation leakage through the shield occurred in the present study, as verified by dose measurement of testis under shielding and morphological structure of peripheral main organs. Meanwhile, Monte Carlo simulation was used to calculate the absorbed dose of the peripheral main organs when mice head was irradiated with 20 Gy X-rays. The results showed that the absorbed dose of testis under shielding was 0.018 Gy, which was only 0.9‰ of cranial absorbed dose. Tandem mass tag (TMT) quantitative proteomic analysis of testis at 4 W after cranial irradiation was carried out by LC-BIO Co., Ltd (Hangzhou, China). The differentially expressed proteins (DEPs) were screened and obtained using the cutoffs of fold change > 1.2 and P < 0.05. For bioinformatics analysis, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed using the DAVID 6.8 database (https://david.ncifcrf.gov/).
2022-10-14 | PXD037407 |
Project description:Cranial irradiation (IR), an effective tool to treat malignant brain tumors, triggers a chronic pro-inflammatory microglial response, at least in the adult brain. Using single cell and bulk RNA sequencing combined with histology, we show that the microglial response in the juvenile mouse hippocampus is rapid, but returns toward normal within 1 week. We found that a single microglial cell simultaneously upregulates transcripts associated with pro- and anti-inflammatory microglial phenotypes. Our results indicate that microglia are involved in the initial stages, but may not be responsible for driving long-term inflammation in the juvenile brain.
2020-06-01 | GSE149247 | GEO
Project description:Cranial radiotherapy induces endocrine disorders and reproductive abnormalities, particularly in long-term female cancer survivors, and this might in part be caused by injury to the pituitary gland, but the underlying mechanisms are unknown. The aim of this study was to investigate the influence of cranial irradiation on the pituitary gland and related endocrine function. Female Wistar rat pups on postnatal day 11 were subjected to a single dose of 6 Gy whole-head irradiation, and hormone levels and organ structure in the reproductive system were examined at 20 weeks after irradiation. We found that brain irradiation reduced cell proliferation and induced persistent inflammation in the pituitary gland. The whole transcriptome analysis of the pituitary gland revealed that apoptosis and inflammation-related pathways were up-regulated after irradiation. In addition, irradiation led to significantly decreased levels of the pituitary hormones, growth hormone, adrenocorticotropic hormone, thyroid-stimulating hormone and the reproductive hormones testosterone and progesterone. To conclude, brain radiation induces reduction of pituitary and reproduction-related hormone secretion, this may due to reduced cell proliferation and increased pituitary inflammation after irradiation. Our results thus provide additional insight into the molecular mechanisms underlying complications after head irradiation and contribute to the discovery of preventive and therapeutic strategies related to brain injury following irradiation.
| S-EPMC7754041 | biostudies-literature
Project description:Cranial and craniospinal irradiation are the oldest central nervous system prophylaxis treatments considered for pediatric patients with acute lymphoblastic leukemia (ALL). However, survivors of childhood ALL that received cranial radiotherapy are at increased risk for deficits in neurocognitive skills. The continuous and dynamic response of normal tissue after irradiation has been identified as one of the causative factors for cognitive changes after cranial radiation therapy. The aim of our study was to investigate the radiation effects on social behavior and neuronal morphology in the hippocampus of adult mice. Twenty-oneday-old male C57BL/6 mice were irradiated with the small-animal radiation research platform (SARRP). Animals were given a single 10-Gy dose of radiation of X-ray cranial radiation. One month following irradiation, animals underwent behavioral testing in the Three-Chamber Sociability paradigm. Radiation affected social discrimination during the third stage eliciting an inability to discriminate between the familiar and stranger mouse, while sham successfully spent more time exploring the novel stranger. Proteomic analysis revealed dysregulation of metabolic and signaling pathways associated with neurocognitive dysfunction such as mitochondrial dysfunction, Rac 1 signaling, and synaptogenesis signaling. We observed significant decreases in mushroom spine density in the Cornu Ammonis 2 of the hippocampus, which is associated with sociability processing.
| S-EPMC7602883 | biostudies-literature
Project description:Irradiation effects on Fasciola hepatica
| PRJEB64689 | ENA
Project description:Fractionated whole-brain irradiation for the treatment of intracranial neoplasia causes progressive neurodegeneration and neuroinflammation. The long-term consequences of high single dose brain irradiation are unknown. In order to assess the late effects of brain irradiation we have compared transcriptomic gene expression profiles from nonhuman primates (rhesus macaques, Macaca mulatta) receiving single dose total body irradiation to those given fractionated whole brain radiotherapy and control comparators. Gene expression profiles from the dorsolateral prefrontal cortex (Brodmann area 46), hippocampus, and deep white matter (centrum semiovale) were compared. The goals of this study were to identify novel potential molecular effects of radiation-induced brain injury, to evaluate regional differences in the cerebral radiation response, and to assess whether animals receiving high dose total body irradiation demonstrated similar transcriptomic patterns as those observed in animals receiving fractionated whole brain irradiation.
2019-03-27 | GSE120901 | GEO
Project description:IntroductionCranial irradiation (IR) negatively regulates hippocampal neurogenesis and causes cognitive dysfunctions in cancer survivors, especially in pediatric patients. IR decreases proliferation of neural stem/progenitor cells (NSPC) and consequently diminishes production of new hippocampal neurons. Memantine, an NMDA receptor antagonist, used clinically to improve cognition in patients suffering from Alzheimer's disease and dementia. In animal models, memantine acts as a potent enhancer of hippocampal neurogenesis. Memantine was recently proposed as an intervention to improve cognitive impairments occurring after radiotherapy and is currently under investigation in a number of clinical trials, including pediatric patients. To date, preclinical studies investigating the mechanisms underpinning how memantine improves cognition after IR remain limited, especially in the young, developing brain. Here, we investigated whether memantine could restore proliferation in the subgranular zone (SGZ) or rescue the reduction in the number of hippocampal young neurons after IR in the juvenile mouse brain.MethodsMice were whole-brain irradiated with 6 Gy on postnatal day 20 (P20) and subjected to acute or long-term treatment with memantine. Proliferation in the SGZ and the number of young neurons were further evaluated after the treatment. We also measured the levels of neurotrophins associated with memantine improved neural plasticity, brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF).ResultsWe show that acute intraperitoneal treatment with a high, non-clinically used, dose of memantine (50 mg/kg) increased the number of proliferating cells in the intact brain by 72% and prevented 23% of IR-induced decrease in proliferation. Long-term treatment with 10 mg/kg/day of memantine, equivalent to the clinically used dose, did not impact proliferation, neither in the intact brain, nor after IR, but significantly increased the number of young neurons (doublecortin expressing cells) with radial dendrites (29% in sham controls and 156% after IR) and enhanced their dendritic arborization. Finally, we found that long-term treatment with 10 mg/kg/day memantine did not affect the levels of BDNF, but significantly reduced the levels of NGF by 40%.ConclusionThese data suggest that the enhanced dendritic complexity of the hippocampal young neurons after treatment with memantine may contribute to the observed improved cognition in patients treated with cranial radiotherapy.
| S-EPMC10584145 | biostudies-literature
Project description:We employ RNA-seq of FACS sorted cell populations to identify genes that are enriched in cranial neural crest in relationship to the trunk. Transcriptional profiling of delaminating cranial and trunk neural crest subpopulations.
2016-06-24 | E-GEOD-75125 | biostudies-arrayexpress