Characterization and classification of rat neural stem cells and differentiated cells by comparative metabolic and lipidomic profiling

Lee, Hwanhui; Lee, Ha-Rim; Kim, Hye-Youn; Lee, Heayyean; Kim, Hyun-Jung; Choi, Hyung‐Kyoon

doi:10.1007/s00216-019-01922-y

Cited by 5 publications

(4 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To explore the role of protein degradation in the control of NSC fate, we treated NSCs with a proteasome inhibitor, MG132, for 48 h in the presence of mitogens, EGF, and FGF2. NSCs are known to proliferate in the presence of growth factors and differentiate into neurons or glia in the absence of growth factors [39][40][41][42]. The ICC data revealed that 100 nM MG132 significantly reduced cell proliferation and induced the percentage of neurons in NSCs, even in the presence of EGF and FGF2 ( Figure 1A,D).…”

Section: Mg132 Increases Neuron Percentage In Rat Nscs In the Presencmentioning

confidence: 94%

Proteasome Inhibitor MG132 is Toxic and Inhibits the Proliferation of Rat Neural Stem Cells but Increases BDNF Expression to Protect Neurons

Kim

2020

Biomolecules

Self Cite

View full text Add to dashboard Cite

Regulation of protein expression is essential for maintaining normal cell function. Proteasomes play important roles in protein degradation and dysregulation of proteasomes is implicated in neurodegenerative disorders. In this study, using a proteasome inhibitor MG132, we showed that proteasome inhibition reduces neural stem cell (NSC) proliferation and is toxic to NSCs. Interestingly, MG132 treatment increased the percentage of neurons in both proliferation and differentiation culture conditions of NSCs. Proteasome inhibition reduced B-cell lymphoma 2 (Bcl-2)/Bcl-2 associated X protein ratio. In addition, MG132 treatment induced cAMP response element-binding protein phosphorylation and increased the expression of brain-derived neurotrophic factor transcripts and proteins. These data suggest that proteasome function is important for NSC survival and differentiation. Moreover, although MG132 is toxic to NSCs, it may increase neurogenesis. Therefore, by modifying MG132 chemical structure and developing none toxic proteasome inhibitors, neurogenic chemicals can be developed to control NSC cell fate.

show abstract

Section: Mg132 Increases Neuron Percentage In Rat Nscs In the Presencmentioning

confidence: 94%

Proteasome Inhibitor MG132 is Toxic and Inhibits the Proliferation of Rat Neural Stem Cells but Increases BDNF Expression to Protect Neurons

Kim

2020

Biomolecules

Self Cite

View full text Add to dashboard Cite

show abstract

“…Specific metabolite levels were observed to significantly vary both between NSCs and OECs, and between NSCs of different ages, with the results presenting potential usefulness in monitoring SC properties in different environments or in pathological conditions (e.g., ageing and neurodegeneration). A second recent report was based on GC-MS and direct infusion (DI)-MS [90] to analyze both the polar and lipid metabolomes of rat NSCs (which proliferate in the presence of growth factors) and differentiated cells (DCs, neurons and glia, win the absence of growth factors). Markedly distinct metabolic profiles were noted between NSCs and DCs, involving six lipids, together with creatinine, lactate, lysine, glutamine, glycine and pyroglutamate, such knowledge potentially aiding in the classification of NSCs and DCs in therapeutics of neurological disorders.…”

Section: Differentiationmentioning

confidence: 99%

Metabolomic Applications in Stem Cell Research: a Review

Bispo

Jesus

Marques

et al. 2021

Stem Cell Rev and Rep

View full text Add to dashboard Cite

This review describes the use of metabolomics to study stem cell (SC) characteristics and function (excluding SCs in cancer research, suited to a fully dedicated text). The interest in employing metabolomics in SC research has consistently grown and emphasis is, here, given to developments reported in the past five years. This text informs on the existing methodologies and their complementarity regarding the information provided, comprising untargeted/targeted approaches, which couple mass spectrometry or nuclear magnetic resonance spectroscopy with multivariate analysis (and, in some cases, pathway analysis and integration with other omics), and more specific analytical approaches, namely isotope tracing to highlight particular metabolic pathways, or in tandem microscopic strategies to pinpoint characteristics within a single cell. The bulk of this review covers the existing applications in various aspects of mesenchymal SC behavior, followed by pluripotent and neural SCs, with a few reports addressing other SC types. Some of the central ideas investigated comprise the metabolic/biological impacts of different tissue/donor sources and differentiation conditions, including the importance of considering 3D culture environments, mechanical cues and/or media enrichment to guide differentiation into specific lineages. Metabolomic analysis has considered cell endometabolomes and exometabolomes (fingerprinting and footprinting, respectively), having measured both lipid species and polar metabolites involved in a variety of metabolic pathways. This review clearly demonstrates the current enticing promise of metabolomics in significantly contributing towards a deeper knowledge on SC behavior, and the discovery of new biomarkers of SC behavior and function with potential translation to in vivo clinical practice.

show abstract

“…Metabolomic analysis has emerged as a powerful research tool to understand the underlying mechanisms of unique features in various cell types [12,13]. Umemura et al analyzed the metabolites of CD11b + splenocytes and tumor-infiltrated macrophages, which are cell types related to MDSCs, by capillary electrophoresis-time-of-flight-mass spectrometry [14].…”

Section: Introductionmentioning

confidence: 99%

Discovery of Myeloid-Derived Suppressor Cell-Specific Metabolism by Metabolomic and Lipidomic Profiling

et al. 2023

Self Cite

View full text Add to dashboard Cite

The endogenous factors that control the differentiation of myeloid-derived suppressor cells (MDSCs) are not yet fully understood. The purpose of this study was to find MDSC-specific biomolecules through comprehensive metabolomic and lipidomic profiling of MDSCs from tumor-bearing mice and to discover potential therapeutic targets for MDSCs. Partial least squares discriminant analysis was performed on the metabolomic and lipidomic profiles. The results showed that inputs for the serine, glycine, and one-carbon pathway and putrescine are increased in bone marrow (BM) MDSC compared to normal BM cells. Splenic MDSC showed an increased phosphatidylcholine to phosphatidylethanolamine ratio and less de novo lipogenesis products, despite increased glucose concentration. Furthermore, tryptophan was found to be at the lowest concentration in splenic MDSC. In particular, it was found that the concentration of glucose in splenic MDSC was significantly increased, while that of glucose 6-phosphate was not changed. Among the proteins involved in glucose metabolism, GLUT1 was overexpressed during MDSC differentiation but decreased through the normal maturation process. In conclusion, high glucose concentration was found to be an MDSC-specific feature, and it was attributed to GLUT1 overexpression. These results will help to develop new therapeutic targets for MDSCs.

show abstract

Characterization and classification of rat neural stem cells and differentiated cells by comparative metabolic and lipidomic profiling

Cited by 5 publications

References 50 publications

Proteasome Inhibitor MG132 is Toxic and Inhibits the Proliferation of Rat Neural Stem Cells but Increases BDNF Expression to Protect Neurons

Proteasome Inhibitor MG132 is Toxic and Inhibits the Proliferation of Rat Neural Stem Cells but Increases BDNF Expression to Protect Neurons

Metabolomic Applications in Stem Cell Research: a Review

Discovery of Myeloid-Derived Suppressor Cell-Specific Metabolism by Metabolomic and Lipidomic Profiling

Contact Info

Product

Resources

About