scholarly journals Isolation of Human Neural Stem Cells from the Amniotic Fluid with Diagnosed Neural Tube Defects

2015 ◽  
Vol 24 (15) ◽  
pp. 1740-1750 ◽  
Author(s):  
Yu-Jen Chang ◽  
Hong-Lin Su ◽  
Lee-Feng Hsu ◽  
Po-Jui Huang ◽  
Tzu-Hao Wang ◽  
...  
2013 ◽  
Vol 22 (4) ◽  
pp. 548-553 ◽  
Author(s):  
Christopher G. Turner ◽  
Justin D. Klein ◽  
Junmei Wang ◽  
Devang Thakor ◽  
Darcy Benedict ◽  
...  

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Xian Li ◽  
Wenjuan Zhou ◽  
Xinyue Li ◽  
Ming Gao ◽  
Shufang Ji ◽  
...  

Abstract Objective Neural tube defects (NTDs) are the most serious and common birth defects in the clinic. The SRY-related HMG box B1 (SoxB1) gene family has been implicated in different processes of early embryogenesis. Sox19b is a maternally expressed gene in the SoxB1 family that is found in the region of the presumptive central nervous system (CNS), but its role and mechanism in embryonic neural stem cells (NSCs) during neural tube development have not yet been explored. Considering that Sox19b is specific to bony fish, we intended to investigate the role and mechanism of Sox19b in neural tube development in zebrafish embryos. Material and methods Morpholino (MO) antisense oligonucleotides were used to construct a Sox19b loss-of-function zebrafish model. The phenotype and the expression of related genes were analysed by in situ hybridization and immunolabelling. Epigenetic modifications were detected by western blot and chromatin immunoprecipitation. Results In this study, we found that zebrafish embryos exhibited a reduced or even deleted forebrain phenotype after the expression of the Sox19b gene was inhibited. Moreover, we found for the first time that knockdown of Sox19b reduced the proliferation of NSCs; increased the transcription levels of Ngn1, Ascl1, HuC, Islet1, and cyclin-dependent kinase (CDK) inhibitors; and led to premature differentiation of NSCs. Finally, we found that knockdown of Sox19b decreased the levels of EZH2/H3K27me3 and decreased the level of H3K27me3 at the promoters of Ngn1 and ascl1a. Conclusion Together, our data demonstrate that Sox19b plays an essential role in early NSC proliferation and differentiation through EZH2-mediated histone methylation in neural tube development. This study established the role of transcription factor Sox19b and epigenetic factor EZH2 regulatory network on NSC development, which provides new clues and theoretical guidance for the clinical treatment of neural tube defects.


2014 ◽  
Vol 37 (1) ◽  
pp. 65-69 ◽  
Author(s):  
Elliot C. Pennington ◽  
Kristy L. Rialon ◽  
Beatrice Dionigi ◽  
Azra Ahmed ◽  
David Zurakowski ◽  
...  

Purpose: The proportions of select stem cells in term amniotic fluid have been shown to correlate with the type and size of experimental neural tube defects (NTDs). We sought to determine the impact of gestational age upon this form of targeted amniotic cell profiling. Methods: Sprague-Dawley fetuses with retinoic acid-induced NTDs (n = 110) underwent amniotic fluid procurement at four time points in gestation. Samples were analyzed by flow cytometry for the presence of cells concomitantly expressing Nestin and Sox-2 (neural stem cells, aNSCs) and cells concomitantly expressing CD29 and CD44 (mesenchymal stem cells, aMSCs). Statistical analysis was by nonparametric Kruskal-Wallis ANOVA (p < 0.05). Results: There was a statistically significant impact of gestational age on the proportions of both aMSCs (p = 0.01) and aNSCs (p < 0.01) in fetuses with isolated spina bifida. No such impact was noted in normal fetuses (p > 0.10 for both cells), in isolated exencephaly (p > 0.10 for both cells), or in combination defects (p > 0.10 for both cells). Gestational age had no effect on aNSC/aMSC ratios. Conclusions: Targeted quantitative amniotic cell profiling varies with gestational age in experimental isolated spina bifida. This finding should be considered prior to the eventual translation of this diagnostic adjunct into the prenatal evaluation of these anomalies.


Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 1043 ◽  
Author(s):  
Phil Jun Kang ◽  
Daryeon Son ◽  
Tae Hee Ko ◽  
Wonjun Hong ◽  
Wonjin Yun ◽  
...  

Human neural stem cells (NSCs) hold enormous promise for neurological disorders, typically requiring their expandable and differentiable properties for regeneration of damaged neural tissues. Despite the therapeutic potential of induced NSCs (iNSCs), a major challenge for clinical feasibility is the presence of integrated transgenes in the host genome, contributing to the risk for undesired genotoxicity and tumorigenesis. Here, we describe the advanced transgene-free generation of iNSCs from human urine-derived cells (HUCs) by combining a cocktail of defined small molecules with self-replicable mRNA delivery. The established iNSCs were completely transgene-free in their cytosol and genome and further resembled human embryonic stem cell-derived NSCs in the morphology, biological characteristics, global gene expression, and potential to differentiate into functional neurons, astrocytes, and oligodendrocytes. Moreover, iNSC colonies were observed within eight days under optimized conditions, and no teratomas formed in vivo, implying the absence of pluripotent cells. This study proposes an approach to generate transplantable iNSCs that can be broadly applied for neurological disorders in a safe, efficient, and patient-specific manner.


2021 ◽  
Vol 22 (8) ◽  
pp. 3913
Author(s):  
Satoshi Nakata ◽  
Ming Yuan ◽  
Jeffrey A. Rubens ◽  
Ulf D. Kahlert ◽  
Jarek Maciaczyk ◽  
...  

Central nervous system tumor with BCL6-corepressor internal tandem duplication (CNS-BCOR ITD) is a malignant entity characterized by recurrent alterations in exon 15 encoding the essential binding domain for the polycomb repressive complex (PRC). In contrast to deletion or truncating mutations seen in other tumors, BCOR expression is upregulated in CNS-BCOR ITD, and a distinct oncogenic mechanism has been suggested. However, the effects of this change on the biology of neuroepithelial cells is poorly understood. In this study, we introduced either wildtype BCOR or BCOR-ITD into human and murine neural stem cells and analyzed them with quantitative RT-PCR and RNA-sequencing, as well as growth, clonogenicity, and invasion assays. In human cells, BCOR-ITD promoted derepression of PRC2-target genes compared to wildtype BCOR. A similar effect was found in clinical specimens from previous studies. However, no growth advantage was seen in the human neural stem cells expressing BCOR-ITD, and long-term models could not be established. In the murine cells, both wildtype BCOR and BCOR-ITD overexpression affected cellular differentiation and histone methylation, but only BCOR-ITD increased cellular growth, invasion, and migration. BCOR-ITD overexpression drives transcriptional changes, possibly due to altered PRC function, and contributes to the oncogenic transformation of neural precursors.


2013 ◽  
Vol 2 (10) ◽  
pp. 731-744 ◽  
Author(s):  
Christopher J. Sontag ◽  
Hal X. Nguyen ◽  
Noriko Kamei ◽  
Nobuko Uchida ◽  
Aileen J. Anderson ◽  
...  

2012 ◽  
Vol 4 (155) ◽  
pp. 155ra136-155ra136 ◽  
Author(s):  
N. Uchida ◽  
K. Chen ◽  
M. Dohse ◽  
K. D. Hansen ◽  
J. Dean ◽  
...  

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