Autocrine glutamatergic transmission for the regulation of embryonal carcinoma stem cells

Teng, Lin; Lei, Hui‐Min; Sun, Fan; An, Shi-Min; Tang, Ya‐Bin; Meng, Shuang; Wang, Conghui; Shen, Ying; Chen, Hongzhuan; Zhu, Liang

doi:10.18632/oncotarget.9973

Cited by 5 publications

(2 citation statements)

References 57 publications

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“…Excitotoxicity, excessive and pathological stimulation of neurons, associated with neuronal death in many neurological diseases, including ischaemia, traumatic brain injury, and neurodegenerative diseases ( Connolly et al, 2016 ; Krasil'nikova et al, 2019 ). All intercellular signaling is dependent on chemical signals, and glutamate is one of the most important intercellular chemical signals in the nervous system ( Özel et al, 2014 ; Teng et al, 2016 ).…”

Section: Glutamate Receptor-mediated Excitotoxicitymentioning

confidence: 99%

The initiator of neuroexcitotoxicity and ferroptosis in ischemic stroke: Glutamate accumulation

Fan

Liu

et al. 2023

Front. Mol. Neurosci.

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Glutamate plays an important role in excitotoxicity and ferroptosis. Excitotoxicity occurs through over-stimulation of glutamate receptors, specifically NMDAR, while in the non-receptor-mediated pathway, high glutamate concentrations reduce cystine uptake by inhibiting the System Xc-, leading to intracellular glutathione depletion and resulting in ROS accumulation, which contributes to increased lipid peroxidation, mitochondrial damage, and ultimately ferroptosis. Oxidative stress appears to crosstalk between excitotoxicity and ferroptosis, and it is essential to maintain glutamate homeostasis and inhibit oxidative stress responses in vivo. As researchers work to develop natural compounds to further investigate the complex mechanisms and regulatory functions of ferroptosis and excitotoxicity, new avenues will be available for the effective treatment of ischaemic stroke. Therefore, this paper provides a review of the molecular mechanisms and treatment of glutamate-mediated excitotoxicity and ferroptosis.

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Section: Glutamate Receptor-mediated Excitotoxicitymentioning

confidence: 99%

The initiator of neuroexcitotoxicity and ferroptosis in ischemic stroke: Glutamate accumulation

Fan

Liu

et al. 2023

Front. Mol. Neurosci.

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“…VGLUT expression in liver, stomach, testis, and platelets suggests that they have numerous functions in the physiology of these sites ( 152 – 154 ). There is evidence of VGLUT expression in carcinoma stem cells that correlates with enhanced release of glutamate and cell proliferation via activation of NMDA receptors ( 155 ); therefore, VGLUT functions could also be implicated in cancer development.…”

Section: Glutamate Signaling In Cancer Of Non-neural Organsmentioning

confidence: 99%

Glutamatergic system components as potential biomarkers and therapeutic targets in cancer in non-neural organs

et al. 2022

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Glutamate is one of the most abundant amino acids in the blood. Besides its role as a neurotransmitter in the brain, it is a key substrate in several metabolic pathways and a primary messenger that acts through its receptors outside the central nervous system (CNS). The two main types of glutamate receptors, ionotropic and metabotropic, are well characterized in CNS and have been recently analyzed for their roles in non-neural organs. Glutamate receptor expression may be particularly important for tumor growth in organs with high concentrations of glutamate and might also influence the propensity of such tumors to set metastases in glutamate-rich organs, such as the liver. The study of glutamate transporters has also acquired relevance in the physiology and pathologies outside the CNS, especially in the field of cancer research. In this review, we address the recent findings about the expression of glutamatergic system components, such as receptors and transporters, their role in the physiology and pathology of cancer in non-neural organs, and their possible use as biomarkers and therapeutic targets.

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Metabolic shift in density-dependent stem cell differentiation

et al. 2017

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BackgroundVascular progenitor cells (VPCs) derived from embryonic stem cells (ESCs) are a valuable source for cell- and tissue-based therapeutic strategies. During the optimization of endothelial cell (EC) inductions from mouse ESCs using our staged and chemically-defined induction methods, we found that cell seeding density but not VEGF treatment between 10 ng/mL and 40 ng/mL was a significant variable directing ESCs into FLK1+ VPCs during stage 1 induction. Here, we examine potential contributions from cell-to-cell signaling or cellular metabolism in the production of VPCs from ESCs seeded at different cell densities.MethodsUsing 1D 1H-NMR spectroscopy, transcriptomic arrays, and flow cytometry, we observed that the density-dependent differentiation of ESCs into FLK1+ VPCs positively correlated with a shift in metabolism and cellular growth.ResultsSpecifically, cell differentiation correlated with an earlier plateauing of exhaustive glycolysis, decreased lactate production, lower metabolite consumption, decreased cellular proliferation and an increase in cell size. In contrast, cells seeded at a lower density of 1,000 cells/cm2 exhibited increased rates of glycolysis, lactate secretion, metabolite utilization, and proliferation over the same induction period. Gene expression analysis indicated that high cell seeding density correlated with up-regulation of several genes including cell adhesion molecules of the notch family (NOTCH1 and NOTCH4) and cadherin family (CDH5) related to vascular development.ConclusionsThese results confirm that a distinct metabolic phenotype correlates with cell differentiation of VPCs.

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Autocrine glutamatergic transmission for the regulation of embryonal carcinoma stem cells

Cited by 5 publications

References 57 publications

The initiator of neuroexcitotoxicity and ferroptosis in ischemic stroke: Glutamate accumulation

The initiator of neuroexcitotoxicity and ferroptosis in ischemic stroke: Glutamate accumulation

Glutamatergic system components as potential biomarkers and therapeutic targets in cancer in non-neural organs

Metabolic shift in density-dependent stem cell differentiation

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