Human mesenchymal stem cells prevent neurological complications of radiotherapy
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA475889 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Radiotherapy is a highly effective tool for the treatment of brain cancer. However, radiation also causes detrimental effects in the healthy tissue, leading to neurocognitive sequelae that compromise the quality of life of brain cancer survivors. Despite the recognition of this serious complication, no satisfactory solutions exist at present. Here we investigated the effects of intranasal administration of human mesenchymal stem cell (hMSCs) as a neuroprotective strategy for cranial radiation in mice. Our results demonstrated that intranasally delivered hMSCs promote radiation-induced brain injury repair, improving neurological function. The molecular analysis revealed that hMSC administration reduces persistent activation of damage-induced c-AMP response element-binding signaling in the irradiated neurogenic niches. Furthermore, hMSC treatment did not compromise survival of glioma-bearing mice. Our findings encourage the therapeutic use of hMSCs as an effective and non-invasive approach to prevent neurological complications of radiotherapy, improving the quality of life of brain tumor survivors.
2019-06-21 | GSE115735 | GEO
Project description:Radiotherapy is a highly effective tool for the treatment of brain cancer. However, radiation also causes detrimental effects in the healthy tissue, leading to neurocognitive sequelae that compromise the quality of life of brain cancer patients. Despite the recognition of this serious complication, no satisfactory solutions exist at present. Here we investigated the effects of intranasal administration of human mesenchymal stem cells (hMSCs) as a neuroprotective strategy for cranial radiation in mice. Our results demonstrated that intranasally delivered hMSCs promote radiation-induced brain injury repair, improving neurological function. This intervention confers protection against inflammation, oxidative stress, and neuronal loss. hMSC administration reduces persistent activation of damage-induced c-AMP response element-binding signaling in irradiated brains. Furthermore, hMSC treatment did not compromise the survival of glioma-bearing mice. Our findings encourage the therapeutic use of hMSCs as a non-invasive approach to prevent neurological complications of radiotherapy, improving the quality of life of brain tumor patients.
| S-EPMC6532528 | biostudies-literature
Project description:Tuberculous meningitis (TBM) is the most severe and deadly manifestation of tuberculosis. Neurological complications, e.g., hydrocephalus are observed in up to 50% of patients affected. The study of TBM pathogenesis is hampered, at least partially, by a lack of experimental models that recapitulate all clinical features of the human disease. With single-cell transcriptome of blood in tuberculosis revealed, the single cell transcriptome atlas in TBM brain remains yet to be explored. Here, a TBM model was built and then whole brain was dissected for single cell sequencing. Transcriptional changes were observed in all cell types, suggesting a complex biology in TBM pathogenesis. As a result, pervasive immune response was activated by transcription factors Stat1 and IRF1 in macrophages and microglia. For neurons, decreased oxidative phosphorylation activity in neurons links TBM with neurodegenerative diseases. Finally, Ependymal cells show most remarkable transcriptional changes, and decreased Frmd4a may contribute to hydrocephalus and neurodegenerative disorders. We first revealed a comprehensive transcriptome map in TBM mouse model with ScRNA-Seq, and link the cell types, transcriptional genes with regulons and functional processes with neurological complications. These identified cellular and molecular changes offer an unprecedented clue for inspiring the clinical diagnosis and therapeutics of TBM.
2023-08-02 | GSE199649 | GEO
Project description:Single cell analysis reveals transcriptional changes underlying neurological complications in tuberculous meningitis
| PRJNA821073 | ENA
Project description:The study of new biomarkers for early detection of diabetes complications could bring new prevent approaches perspectives.
2023-05-11 | E-MTAB-13000 | biostudies-arrayexpress
Project description:Patients treated with radiotherapy to the chest region are at risk of cardiac sequelae, however, identification of those with greatest risk of complications remains difficult. Here, we sought to determine whether short-term changes in circulating miRNA expression are related to measures of cardiac dysfunction in follow-up. miRNA expression analysis in the primary group showed marked changes in serum miRNAs immediately after RT compared to baseline. miRNAs with increased expression correlated positively with cardiopulmonary dose-volume histogram metrics, while those with decreased expression exhibited negative correlations.
2023-05-07 | GSE225243 | GEO
Project description:Dog neurological disease-identification of mutation
| PRJEB71373 | ENA
Project description:We report major tumor regressions in a subset of advanced cancer patients for which cold tumors were treated with low-dose radiotherapy, cyclophosphamide, aspirin, and ICB (NCT03728179). Unbiased analyses of biopsies revealed T-cell infiltration, up-regulation of type I IFN, and Th1 signatures as well as down-regulation of M2 macrophage and epithelial to mesenchymal transition gene-signatures, and a more oligoclonal TCR repertoire after radio-combinatorial immunotherapy, in responding patients.
2021-08-16 | GSE167455 | GEO
Project description:Roseburia sensitizes colorectal cancer to radiotherapy
| PRJEB45422 | ENA
Project description:Immune checkpoint blockade is a powerful oncologic treatment modality for a wide variety of human malignancies. Randomized clinical trials are assessing how best to interdigitate this treatment modality with traditional therapies including radiotherapy. A challenge in oncology is to rationally and effectively integrate immunotherapy with traditional modalities including radiotherapy. Here, we demonstrate that radiotherapy induces tumor cell ferroptosis. Ferroptosis agonists augment and ferroptosis antagonists limit radiotherapy efficacy in tumor models. Immunotherapy sensitizes tumors to radiotherapy by promoting tumor cell ferroptosis. Mechanistically, IFN derived from immunotherapy-activated CD8+ T cells and radiotherapy-activated ATM independently, yet synergistically repress SLC7A11, a unit of the glutamate-cystine antiporter xc-, resulting in reduced cystine uptake, enhanced tumor lipid oxidation and ferroptosis, and improved tumor control. Thus, ferroptosis is an unappreciated mechanism and focus for the development of effective combinatorial cancer therapy.
2020-09-23 | GSE137946 | GEO