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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

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			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

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

Project description:Osteoradionecrosis of the jaw (ORNJ) is a complication after head and neck radiotherapy. 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 metabolome. Compared to the unirradiated BMSCs, the taurine content of irradiated BMSCs decreases, and the taurine uptake 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 and decreases the generation of reactive oxygen species (ROS) of irradiated BMSCs. Oral administration of taurine significantly promotes osteogenesis of irradiated jaws and alleviates bone marrow fibrosis. 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.

2024-11-18 | GSE269255 | GEO

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.

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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.

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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.

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

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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.

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