NG2 cells and their neurogenic potential

2020 ◽  
Vol 50 ◽  
pp. 53-60 ◽  
Author(s):  
Denisa Kirdajova ◽  
Miroslava Anderova
Keyword(s):  
Ng2 Cells

scholarly journals Cell cycle dynamics of NG2 cells in the postnatal and ageing brain

2009 ◽  
Vol 5 (3-4) ◽  
pp. 57-67 ◽  
Author(s):  
Konstantina Psachoulia ◽  
Francoise Jamen ◽  
Kaylene M. Young ◽  
William D. Richardson
Keyword(s):  
Cell Cycle ◽  
Corpus Callosum ◽  
Biological Significance ◽  
Growth Fraction ◽  
Cell Cycle Time ◽  
Active Population ◽  
Dorsal Telencephalon ◽  
Ng2 Cells ◽  
Cell Cycle Dynamics ◽  
Ageing Brain

Oligodendrocyte precursors (OLPs or ‘NG2 cells’) are abundant in the adult mouse brain, where they continue to proliferate and generate new myelinating oligodendrocytes. By cumulative BrdU labelling, we estimated the cell cycle timeTCand the proportion of NG2 cells that is actively cycling (the growth fraction) at ~ postnatal day 6 (P6), P60, P240 and P540. In the corpus callosum,TCincreased from <2 days at P6 to ~9 days at P60 to ~70 days at P240 and P540. In the cortex,TCincreased from ~2 days to >150 days over the same period. The growth fraction remained relatively invariant at ~50% in both cortex and corpus callosum – that is, similar numbers of mitotically active and inactive NG2 cells co-exist at all ages. Our data imply that a stable population of quiescent NG2 cells appears before the end of the first postnatal week and persists throughout life. The mitotically active population acts as a source of new oligodendrocytes during adulthood, while the biological significance of the quiescent population remains to be determined. We found that the mitotic status of adult NG2 cells is unrelated to their developmental site of origin in the ventral or dorsal telencephalon. We also report that new oligodendrocytes continue to be formed at a slow rate from NG2 cells even after P240 (8 months of age).

Abstract MP123: The Fate and Role of Pericytes in Repair and Remodeling of the Infarcted Heart

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Linda Alex ◽  
Ya Su ◽  
Nikolaos G Frangogiannis
Keyword(s):  
Lineage Tracing ◽  
Mrna Levels ◽  
Infarct Zone ◽  
Subsequent Formation ◽  
Mural Cells ◽  
Infarcted Heart ◽  
Reporter Mice ◽  
Ng2 Cells ◽  
Migratory Phenotype

Repair of the infarcted heart is dependent on inflammation-driven activation of myofibroblasts (MFs) and subsequent formation of a scar. Though pericytes have been implicated in injury-associated fibroblast activation in several organs, their potential role in cardiac repair and fibrosis has not been studied. We hypothesized that myocardial infarction (MI) may induce pericyte activation, contributing to repair through pericyte to MF conversion, secretion of fibrogenic mediators, or regulation of angiogenesis. In order to test the hypothesis, we generated pericyte/fibroblast reporter mice (NG2 DsRed ;PDGFRα GFP ). In normal myocardium, NG2 labeled peri-endothelial mural cells that coexpressed PDGFRβ, whereas PDGFRα identified interstitial cells with fibroblast characteristics. Pericytes and fibroblasts had distinct transcriptomic profiles: NG2+/PDGFRα- pericytes expressed αSMA and low amounts of extracellular matrix (ECM) genes, whereas PDGFRα+/NG2- fibroblasts synthesized collagens. Pericyte rarefaction was noted in the necrotic core 3 days after non-reperfused MI. 3-7 days post MI, expansion of the NG2+ population in the infarct zone was associated with emergence of non-mural NG2+/αSMA+ cells with MF characteristics. FACS-sorted NG2+/PDGFRα- cells from 7-day infarcts expressed higher levels of ColIα2 (7.2±1.0-fold) and ColIIIα1 (8.9±1.14-fold), when compared to NG2+/PDGFRα- cells from normal hearts. NG2+ cells had high mRNA levels of integrins α1, αV, β1, and β5, and of MMP14, reflecting an activated migratory phenotype. To examine whether expression of ECM genes by infarct pericytes is due to fibroblast conversion, we did lineage tracing studies using NG2CreER TM ;Rosa tdTomato mice bred with the PDGFRα GFP line for reliable fibroblast identification. 7 days post MI, 5.7%±1.04 of PDGFRα+ fibroblasts were derived from NG2+ cells. Also, αSMA staining showed that 10.49%±2.73 of infarct MFs were derived from NG2+ lineage. The majority of mural cells wrapping neovessels were derived from NG2+ cells, suggesting a role for resident pericytes in infarct angiogenesis. In conclusion, upon MI, pericytes become activated and contribute to repair by undergoing conversion to a subset of myofibroblasts and by coating infarct neovessels.

scholarly journals A non-hierarchical organization of tumorigenic NG2 cells in glioblastoma promoted by EGFR

2018 ◽  
Vol 21 (6) ◽  
pp. 719-729 ◽  
Author(s):  
Talal F Al-Mayhani ◽  
Richard M Heywood ◽  
Vamsidhara Vemireddy ◽  
Justin D Lathia ◽  
Sara G M Piccirillo ◽  
...  
Keyword(s):  
Growth Factor Receptor ◽  
Hierarchical Organization ◽  
Egfr Signaling ◽  
Resistant Disease ◽  
Egfr Expression ◽  
Ng2 Cells ◽  
Human Gbm ◽  
Rna Knockdown ◽  
Cellular Hierarchy ◽  
Relationship Of

Abstract Background Expression of neuron-glial antigen 2 (NG2) identifies an aggressive malignant phenotype in glioblastoma (GBM). Mouse models have implicated NG2 in the genesis, evolution, and maintenance of glial cancers and have highlighted potential interactions between NG2 and epidermal growth factor receptor (EGFR). However, it is unknown whether the lineage relationship of NG2+ and NG2− cells follows a hierarchical or stochastic mode of growth. Furthermore, the interaction between NG2 and EGFR signaling in human GBM is also unclear. Methods Single GBM NG2+ and NG2− cells were studied longitudinally to assess lineage relationships. Short hairpin RNA knockdown of NG2 was used to assess the mechanistic role of NG2 in human GBM cells. NG2+ and NG2− cells and NG2 knockdown (NG2-KD) and wild type (NG2-WT) cells were analyzed for differential effects on EGFR signaling. Results Expression of NG2 endows an aggressive phenotype both at single cell and population levels. Progeny derived from single GBM NG2− or GBM NG2+ cells consistently establish phenotypic equilibrium, indicating the absence of a cellular hierarchy. NG2 knockdown reduces proliferation, and mice grafted with NG2-KD survive longer than controls. Finally, NG2 promotes EGFR signaling and is associated with EGFR expression. Conclusions These data support a dynamic evolution in which a bidirectional relationship exists between GBM NG2+ and GBM NG2− cells. Such findings have implications for understanding phenotypic heterogeneity, the emergence of resistant disease, and developing novel therapeutics.

scholarly journals Pro-Inflammatory Cytokines Reduce the Proliferation of NG2 Cells and Increase Shedding of NG2 In Vivo and In Vitro

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e109387 ◽  
Author(s):  
Malin Wennström ◽  
Shorena Janelidze ◽  
Cecilie Bay-Richter ◽  
Lennart Minthon ◽  
Lena Brundin
Keyword(s):  
Inflammatory Cytokines ◽  
Ng2 Cells ◽  
Pro Inflammatory Cytokines

scholarly journals NG2 cells (polydendrocytes): Listeners to the neural network with diverse properties

Glia ◽  
2014 ◽  
Vol 62 (8) ◽  
pp. 1195-1210 ◽  
Author(s):  
Robert A. Hill ◽  
Akiko Nishiyama
Keyword(s):  
Neural Network ◽  
The Neural Network ◽  
Ng2 Cells

scholarly journals NG2 cells: Properties, progeny and origin

2010 ◽  
Vol 63 (1-2) ◽  
pp. 72-82 ◽  
Author(s):  
Jacqueline Trotter ◽  
Khalad Karram ◽  
Akiko Nishiyama
Keyword(s):  
Ng2 Cells

scholarly journals Ca2+ signaling evoked by activation of Na+ channels and Na+/Ca2+ exchangers is required for GABA-induced NG2 cell migration

2009 ◽  
Vol 186 (1) ◽  
pp. 113-128 ◽  
Author(s):  
Xiao-ping Tong ◽  
Xiang-yao Li ◽  
Bing Zhou ◽  
Wanhua Shen ◽  
Zhi-jun Zhang ◽  
...  
Keyword(s):  
Gabaa Receptors ◽  
Physiological Role ◽  
Brain Regions ◽  
Na Channels ◽  
Typical Action ◽  
Sequential Activation ◽  
Ng2 Cells ◽  
And Function ◽  
Ca2 Channels

NG2 cells originate from various brain regions and migrate to their destinations during early development. These cells express voltage-gated Na+ channels but fail to produce typical action potentials. The physiological role of Na+ channels in these cells is unclear. We found that GABA induces membrane depolarization and Ca2+ elevation in NG2 cells, a process requiring activation of GABAA receptors, Na+ channels, and Na+/Ca2+ exchangers (NCXs), but not Ca2+ channels. We have identified a persistent Na+ current in these cells that may underlie the GABA-induced pathway of prolonged Na+ elevation, which in turn triggers Ca2+ influx via NCXs. This unique Ca2+ signaling pathway is further shown to be involved in the migration of NG2 cells. Thus, GABAergic signaling mediated by sequential activation of GABAA receptors, noninactivating Na+ channels, and NCXs may play an important role in the development and function of NG2 glial cells in the brain.

scholarly journals NG2 cells are distinct from neurogenic cells in the postnatal mouse subventricular zone

2009 ◽  
Vol 512 (5) ◽  
pp. 702-716 ◽  
Author(s):  
Mila Komitova ◽  
Xiaoqin Zhu ◽  
David R. Serwanski ◽  
Akiko Nishiyama
Keyword(s):  
Subventricular Zone ◽  
Ng2 Cells

Synaptic communication between neurons and NG2+ cells

2006 ◽  
Vol 16 (5) ◽  
pp. 515-521 ◽  
Author(s):  
Martin Paukert ◽  
Dwight E Bergles
Keyword(s):  
Ng2 Cells

Effects of Propofol on the Proliferation and Differentiation of NG2 Cells in the Hippocampus of Aged Rats

2019 ◽  
Vol 9 (8) ◽  
pp. 1058-1064
Author(s):  
Jie Li ◽  
Zhen-Yuan Wang ◽  
Ming-Ying Li ◽  
Miao He ◽  
Xiao-Li Sun ◽  
...  
Keyword(s):  
Neuronal Apoptosis ◽  
Control Group ◽  
Aged Rats ◽  
Shuttle Box ◽  
Sd Rats ◽  
Proliferation And Differentiation ◽  
Gfap Expression ◽  
Group A ◽  
Ng2 Cells ◽  
Control Group Group

Introduction: Anaesthetics can lead to cognitive impairment and partly recover. Whether this process is related to NG2 cells has not been reported. The present study aims to investigate the effects of propofol on the proliferation and differentiation of NG2 cells in the hippocampus of aged rats. Material and Methods: A total of 80 healthy SD rats were used for the investigation. These rats were randomly divided into two groups: control group (group C, n = 20) and anesthetic group (group A, n = 60). Rats in group A were continuously anesthetized by intravenous infusion of propofol for three hours, and underwent shuttle box test at seven days (A7), 14 days (A14) and three months (A3m) after anesthesia. Then, these rats were further divided into two groups: POCD group (three sub-groups: P7 group, P14 group and P3m group) and non-POCD group (three sub-groups: groups NP7, NP14 and NP3m). Results: Compared with group C, NG2 and PCNA cells in group A were upregulated at seven and 14 days after anesthesia. Compared with group C, MAP2 expression was downregulated, and OX42 and GFAP expression was upregulated in the POCD group, while MAP2 expression in the non-POCD group was upregulated. Compared with the non-POCD group, in the NG2 positive cells, MAP2 expression was downregulated, while OX42 and GFAP expression was upregulated in the POCD group, MAP2 expression was urelugated gradually during the 14th days after anesthesia ( P < 0.05 or P <0.01). Conclusions: Propofol induces neuronal apoptosis and the proliferation of NG2 cells. The direction of NG2 cell differentiation may be correlated to the recovery of cognitive dysfunction.

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