Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Taurine ameliorates oxidative stress of BMSCs and promotes osteogenesis in irradiated jaws

ABSTRACT: Osteoradionecrosis of the jaw (ORNJ) is a complication after head and neck radiotherapy that severely affects patients’ quality of life. Currently, an overall understanding of microenvironmental factors of ORNJ is still lacking. Here, we reveal the activation of taurine metabolism in irradiated mandibular stromal cells with scRNA-Seq and the decrease of taurine in irradiated bone marrow mesenchymal stromal cells (BMSCs) with metabolomics. Compared to the unirradiated BMSCs, the taurine uptake of irradiated BMSCs increases. The taurine concentration in peripheral blood and jaws of irradiated mice are significantly lower than the unirradiated mice. Supplementation of taurine promotes osteogenic differentiation, decreases oxidative stress and DNA damage of irradiated BMSCs. Oral administration of taurine significantly promotes survival rate of irradiated mice and promotes osteogenesis of irradiated jaws. Our study sheds light on the role of taurine during the recovery of radiation-induced jaw injury, suggesting a potential non-invasive therapeutic means to combat ORNJ.

INSTRUMENT(S): Liquid Chromatography MS -

SUBMITTER: Heng Chen

PROVIDER: MTBLS10284 | MetaboLights | 2024-07-08

REPOSITORIES: MetaboLights

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	MTBLS10284	Other
	FILES	Other
	a_MTBLS10284_LC-MS___metabolite_profiling-1.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS10284_LC-MS___metabolite_profiling-1_v2_maf.tsv	Tabular

Items per page:

1 - 5 of 6

Similar Datasets

Human mesenchymal stem cells prevent neurological complications of radiotherapy

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

A study on the radiosensitivity of radiation-induced lung injury at the acute phase based on single-cell transcriptomics

Project description:Radiation-induced lung injury (RILI) is the most common complication associated with chest tumors, such as lung and breast cancers, after radiotherapy; however, the pathogenic mechanisms are unclear.Here, a single-cell transcriptome map was established in a mouse model of acute RILI. In total, 18,500 single-cell transcripts were generated, and 10 major cell types were identified. The heterogeneity and radiosensitivity of each cell type or subtype in the lung tissues during the acute stage were revealed. It was found that immune cells had higher radiosensitivity than stromal cells. Immune cells were highly heterogeneous in terms of radiosensitivity, while some immune cells had the characteristics of radiation resistance. Two groups of radiation-induced Cd8+Mki67+ T cells and Cd4+Cxcr6+ helper T cells were identified. In summary, This study investigated the dynamic changes in the cellular microenvironment during acute lung injury.

2022-06-21 | GSE206426 | GEO

Stromal PTEN determines mammary epithelial response to radio-therapy

Project description:It is well-described that the tumor stroma participates in cancer progression, but whether stromal factors can initiate breast tumorigenesis remains unclear. Using our previously described stromal-specific phosphatase and tensin homolog (PTEN) deletion mouse model, we investigated transformative events in young, non-tumor bearing animals. Here, we show stromal PTEN deletion initiates radiation-induced genomic instability on neighboring mammary epithelium through paracrine epidermal growth factor receptor (EGFR) activation. In these mice, a single low dose of whole-body radiation induces mammary hyperplasia, a result that is prevented by pre-treatment with an EGFR inhibitor. We reveal that stromal PTEN is lost in a subset of normal breast samples and is predictive of recurrence in breast cancer patients. Combined, these data suggest both diagnostic and therapeutic chest wall radiotherapy may inadvertently predispose patients with focal stromal PTEN loss to secondary breast cancer, and that this predisposition may be treated prophylactically through EGFR inhibition.

2018-06-13 | GSE93784 | GEO

Protein difference of breast cancer tissue in mice after radiation therapy and without radiation

Project description:In this study, radiation therapy was performed on mouse breast cancer spontaneous gene mice (MMTV-PyMT) to obtain radiation therapy model of breast cancer mice. To simulate clinical breast cancer radiotherapy and study the differential proteins of breast cancer radiotherapy resistance. MMTV-PyMT mice were randomly divided into two groups, and the radiotherapy group was given the same dose 5 times (3GY, once every 2 days) when the breast cancer tumor grew to an appropriate size (200mm3). The protein extracted from mouse tumor was analyzed by mass spectrometry.

2023-12-06 | PXD047555 |

TGFÎ² confers resistance to radiotherapy in non-small cell lung cancer

Project description:Radiotherapy is standard of care for inoperable non-small cell lung cancers (NSCLC) but adenocarcinoma NSCLC respond more poorly than squamous cell NSCLC. Transforming growth factor Î² (TGFÎ²) activity is induced by radiation and plays a recently recognized role in the DNA damage response. Here we show in murine lung tumor model that radiation activates TGFÎ² acutely and persistently and that TGFÎ² neutralizing antibody, 1D11, systemic treatment increased tumor control following either fractionated or single high dose radiation regimes. TGFÎ² dependent genes in the irradiated tumor indicated crosstalk between innate and adaptive immunity but therapeutic benefit of 1D11 in irradiated tumors in immunocompromised mice suggested that innate immune cells are more influential than the adaptive immune response. Irradiated tumors in which TGFÎ² was blocked were highly hypoxic, exhibit pronounced microvascular damage and promoted neither cancer-associated fibroblasts nor recruit bone marrow derived cells (BMDC). Tumor educated immature BMDC were significant sources of TGFÎ² and inhibiting BMDC recruitment achieved tumor growth control in response to RT comparable to TGFÎ² inhibition. Thus, radiation-induced TGFÎ² both compromises tumor control by RT and promotes reestablishment of the tumor microenvironment. Concordant with the critical role of TGFÎ² activity in RT, radiation resistant NSCLC adenocarcinomas exhibit higher TGFÎ² activity compared to squamous cell NSCLC, which suggests a rationale for using TGFÎ² inhibition to augment radiotherapy. Lewis lung cancer (LLC) model were established in 6 to 8 week-old C57BL/6 female mice by subcutaneous injection. When tumors were 60-80 mm3, Mice were randomized to achieve comparable mean tumor size for each treatment group as indicated below. Tumor growth were monitored and tumors were collected and characterized by gene expression profiling and immunostaining.

2015-12-15 | E-GEOD-73095 | biostudies-arrayexpress

Transcription profiling of human breast stroma and epithelium after curative radiotherapy to investigate the pathogenesis of late radiation injury in humans

Project description:Gene expression profiling of normal tissues after curative radiotherapy was carried out to investigate the pathogenesis of late radiation injury in humans. Irradiated and control normal breast tissue was collected from patients undergoing bilateral mastectomy for ipsilateral tumour relapse or prophylaxis following radiotherapy for breast cancer. Using P.A.L.M. laser capture microdissection (LCM) of frozen sections, breast tissue was separated into an epithelial compartment (terminal duct lobular units and ducts) and a stromal compartment (remaining tissue). RNA was extracted, amplified and hybridised to a 20k cDNA array against a breast tissue reference RNA. Expression profiles of irradiated vs control breast were compared for each tissue compartment

2008-08-12 | E-TABM-419 | biostudies-arrayexpress

Tumorgenic properties of high-dose ionizing radiation of primary cancer-associated fibroblasts

Project description:In the context of radiotherapy, the effects elicited by ionizing radiation on the supportive stroma of tumors remains understudied. Tumor infiltrating fibroblasts are abundantly found in the stromal tissue of most tumor types and are key determinants of tumor progression and metastasis. Given the clinical attention that ablative radiotherapy is gaining nowadays, and the paramount role played by CAFs in cancer sustainability, in this study the effect of high-dose ionizing radiation on primary CAF?S have been investigated. We have used high-throughput transcriptome analysis to ascertain in which degree tumor stromal fibroblast become pro-tumorigenic or anti-tumorigenic after ablative irradiation. Hence, genome-wide transcriptome analysis has been carried out on CAFs isolated from NSCLC tumors after receiving a single dose of 18 Gray. The expressions of relevant genes have been validated by real-time PCR, and transformed cellular pathways have been checked by functional assays. Overall, our data reveals profound changes in biological pathways including cellular stress, DNA damage, cell cycle, aging, apoptosis, oxidative stress, and matrix remodeling. Ablative radiation doses may exert both pro-and anti-tumorigenic effects on CAFs. The ultimate effect of such disturbances merits further investigation in more complex in vivo settings.

2012-04-16 | GSE37318 | GEO

CRISPR screen of radiation resistant genes in NSCLC

Project description:Radiotherapy is an important treatment for non-small cell lung cancer (NSCLC). It not only kills tumor cells directly, but also promotes the efficacy of immunotherapy. However, resistance to radiotherapy is still an unavoidable clinical challenge. In this study, we used radiation-sensitive H460 cell line to stably express Cas9 and CRISPR GeCKO v2 library (A and B). Then a single 4GY irradiation was given, and after the cells resumed proliferation, the total genome was extracted and second-generation sequencing was performed. Genes directly associated with resistance to radiotherapy were identified in comparison to controls without any treatment.

2024-07-12 | GSE218225 | GEO

Expression data from distal colorectal tissues of Pdgfc+/+ and Pdgfc-/- mice with or without irradiation

Project description:Radiation therapy for malignancies in the pelvic region leads to a crucial complication called radiation proctopathy(RP) with acute changes in bowel habits or long-term morbidity. We used microarrays to detail the genome-wide profiles of mice with different genotypes (Pdgfc+/+ and Pdgfc-/- ) under irradiation treatment or not.

2021-08-24 | GSE145131 | GEO

The Poly (ADP-Ribose) Polymerase inhibitor Veliparib and Radiation Cause Significant Cell Line Dependent Metabolic Changes in Breast Cancer Cells

Project description:Breast tumors are characterized into different subtypes based on their surface marker expression, which affects their prognosis and treatment. For example, triple negative breast cancer cells (ER-/PR-/Her2-) show reduced susceptibility towards radiotherapy and chemotherapeutic agents. Poly (ADP-ribose) polymerase (PARP) inhibitors have shown promising results in clinical trials, both as single agents and in combination with other chemotherapeutics, in several subtypes of breast cancer patients. PARP1 is involved in DNA repair, apoptosis, and transcriptional regulation and an understanding of the effects of PARP inhibitors, specifically on metabolism, is currently lacking. Here, we have used NMR-based metabolomics to probe the cell line-specific effects of PARP inhibitor and radiation on metabolism in three distinct breast cancer cell lines. Our data reveal several cell line independent metabolic changes upon PARP inhibition, including an increase in taurine. Pathway enrichment and topology analysis identified that nitrogen metabolism, glycine, serine and threonine metabolism, aminoacyl-tRNA biosynthesis and taurine and hypotaurine metabolism were enriched after PARP inhibition in the three breast cancer cell lines. We observed that the majority of metabolic changes due to radiation as well as PARP inhibition were cell line dependent, highlighting the need to understand how these treatments affect cancer cell response via changes in metabolism. Finally, we observed that both PARP inhibition and radiation induced a similar metabolic response in the HCC1937 (BRCA mutant cell line), but not in MCF-7 and MDAMB231 cells, suggesting that radiation and PARP inhibition share similar interactions with metabolic pathways in BRCA mutant cells. Our study emphasizes the importance of differences in metabolic responses to cancer treatments in different subtypes of cancers.

2016-11-07 | MTBLS337 | MetaboLights

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data