Neural differentiation of mouse embryonic stem cells

2003 ◽  
Vol 31 (1) ◽  
pp. 45-49 ◽  
Author(s):  
M.P. Stavridis ◽  
A.G. Smith
Keyword(s):  
Stem Cells ◽  
Central Nervous System ◽  
Nervous System ◽  
Stem Cell ◽  
Embryonic Stem Cells ◽  
Neural Differentiation ◽  
Embryonic Stem ◽  
Cell Replacement ◽  
Quantification Analysis ◽  
The Central Nervous System

Pluripotent embryonic stem cells can give rise to neuroectodermal derivatives in culture. This potential could be harnessed to generate neurons and glia for cell-replacement therapies in the central nervous system and for use in drug discovery. However, current methods of neural differentiation are empirical and relatively innefficient. Here, we review these methodologies and present new tools for quantification, analysis and manipulation of embryonic stem cell neural determination.

Ablation of Tumor-Derived Stem Cells Transplanted to the Central Nervous System by Genetic Modification of Embryonic Stem Cells with a Suicide Gene

2007 ◽  
Vol 18 (12) ◽  
pp. 1182-1192 ◽  
Author(s):  
Juyeon Jung ◽  
Neil R. Hackett ◽  
Robert G. Pergolizzi ◽  
Lorraine Pierre-Destine ◽  
Anja Krause ◽  
...  
Keyword(s):  
Stem Cells ◽  
Central Nervous System ◽  
Nervous System ◽  
Embryonic Stem Cells ◽  
Genetic Modification ◽  
Embryonic Stem ◽  
Suicide Gene ◽  
The Central Nervous System

scholarly journals Epsins Regulate Mouse Embryonic Stem Cell Exit from Pluripotency and Neural Commitment by Controlling Notch Activation

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Marina Cardano ◽  
Jacopo Zasso ◽  
Luca Ruggiero ◽  
Giuseppina Di Giacomo ◽  
Matteo Marcatili ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Embryonic Stem Cells ◽  
Notch Signaling ◽  
Neural Differentiation ◽  
Radial Glia ◽  
Embryonic Stem ◽  
Mouse Embryonic Stem Cell ◽  
Neural Progenitors ◽  
Notch Activation

Epsins are part of the internalization machinery pivotal to control clathrin-mediated endocytosis. Here, we report that epsin family members are expressed in mouse embryonic stem cells (mESCs) and that epsin1/2 knockdown alters both mESC exits from pluripotency and their differentiation. Furthermore, we show that epsin1/2 knockdown compromises the correct polarization and division of mESC-derived neural progenitors and their conversion into expandable radial glia-like neural stem cells. Finally, we provide evidence that Notch signaling is impaired following epsin1/2 knockdown and that experimental restoration of Notch signaling rescues the epsin-mediated phenotypes. We conclude that epsins contribute to control mESC exit from pluripotency and allow their neural differentiation by appropriate modulation of Notch signaling.

scholarly journals Distinct SoxB1 networks are required for naïve and primed pluripotency

2017 ◽  
Author(s):  
Andrea Corsinotti ◽  
Frederick C. K. Wong ◽  
Tülin Tatar ◽  
Iwona Szczerbinska ◽  
Florian Halbritter ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Embryonic Stem Cells ◽  
Cell Fate ◽  
Neural Differentiation ◽  
Embryonic Stem ◽  
Functional Redundancy ◽  
Self Renewal ◽  
Cell Fate Decisions ◽  
Pluripotent State

AbstractDeletion of Sox2 from embryonic stem cells (ESCs) causes trophectodermal differentiation. While this can be prevented by enforced expression of the related SOXB1 proteins, SOX1 or SOX3, the roles of SOXB1 proteins in epiblast stem cell (EpiSC) pluripotency are unknown. Here we show that Sox2 can be deleted from EpiSCs with impunity. This is due to a shift in the balance of SoxB1 expression in EpiSCs, which have decreased Sox2 and increased Sox3 compared to ESCs. Consistent with functional redundancy, Sox3 can also be deleted from EpiSCs without eliminating self-renewal. However, deletion of both Sox2 and Sox3 prevents self-renewal. The overall SOXB1 levels in ESCs affect differentiation choices: neural differentiation of Sox2 heterozygous ESCs is compromised, while increased SOXB1 levels divert the ESC to EpiSC transition towards neural differentiation. Therefore, optimal SOXB1 levels are critical for each pluripotent state and for cell fate decisions during exit from naïve pluripotency.

scholarly journals Distinct SoxB1 networks are required for naïve and primed pluripotency

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Andrea Corsinotti ◽  
Frederick CK Wong ◽  
Tülin Tatar ◽  
Iwona Szczerbinska ◽  
Florian Halbritter ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Embryonic Stem Cells ◽  
Cell Fate ◽  
Neural Differentiation ◽  
Embryonic Stem ◽  
Mouse Embryonic Stem Cells ◽  
Self Renewal ◽  
Cell Fate Decisions ◽  
Pluripotent State

Deletion of Sox2 from mouse embryonic stem cells (ESCs) causes trophectodermal differentiation. While this can be prevented by enforced expression of the related SOXB1 proteins, SOX1 or SOX3, the roles of SOXB1 proteins in epiblast stem cell (EpiSC) pluripotency are unknown. Here, we show that Sox2 can be deleted from EpiSCs with impunity. This is due to a shift in the balance of SoxB1 expression in EpiSCs, which have decreased Sox2 and increased Sox3 compared to ESCs. Consistent with functional redundancy, Sox3 can also be deleted from EpiSCs without eliminating self-renewal. However, deletion of both Sox2 and Sox3 prevents self-renewal. The overall SOXB1 levels in ESCs affect differentiation choices: neural differentiation of Sox2 heterozygous ESCs is compromised, while increased SOXB1 levels divert the ESC to EpiSC transition towards neural differentiation. Therefore, optimal SOXB1 levels are critical for each pluripotent state and for cell fate decisions during exit from naïve pluripotency.

Neural differentiation of embryonic stem cells induced by conditioned medium from neural stem cell

Neuroreport ◽  
2006 ◽  
Vol 17 (10) ◽  
pp. 981-986 ◽  
Author(s):  
Jia-Qing Zhang ◽  
Xin-Bing Yu ◽  
Bao-Feng Ma ◽  
Wei-Hua Yu ◽  
Ai-Xia Zhang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Embryonic Stem Cells ◽  
Conditioned Medium ◽  
Neural Stem Cell ◽  
Neural Differentiation ◽  
Embryonic Stem

scholarly journals Biomaterial Strategies to Bolster Neural Stem Cell-Mediated Repair of the Central Nervous System

2021 ◽  
pp. 1-15
Author(s):  
Giancarlo Tejeda ◽  
Andrew J. Ciciriello ◽  
Courtney M. Dumont
Keyword(s):  
Stem Cells ◽  
Central Nervous System ◽  
Nervous System ◽  
Stem Cell ◽  
Stem Cell Transplant ◽  
Cell Transplant ◽  
Stem Cell Therapies ◽  
Cell Therapies ◽  
Transplant Survival ◽  
The Central Nervous System

Stem cell therapies have the potential to not only repair, but to regenerate tissue of the central nervous system (CNS). Recent studies demonstrate that transplanted stem cells can differentiate into neurons and integrate with the intact circuitry after traumatic injury. Unfortunately, the positive findings described in rodent models have not been replicated in clinical trials, where the burden to maintain the cell viability necessary for tissue repair becomes more challenging. Low transplant survival remains the greatest barrier to stem cell-mediated repair of the CNS, often with fewer than 1–2% of the transplanted cells remaining after 1 week. Strategic transplantation parameters, such as injection location, cell concentration, and transplant timing achieve only modest improvements in stem cell transplant survival and appear inconsistent across studies. Biomaterials provide researchers with a means to significantly improve stem cell transplant survival through two mechanisms: (1) a vehicle to deliver and protect the stem cells and (2) a substrate to control the cytotoxic injury environment. These biomaterial strategies can alleviate cell death associated with delivery to the injury and can be used to limit cell death after transplantation by limiting cell exposure to cytotoxic signals. Moreover, it is likely that control of the injury environment with biomaterials will lead to a more reliable support for transplanted cell populations. This review will highlight the challenges associated with cell delivery in the CNS and the advances in biomaterial development and deployment for stem cell therapies necessary to bolster stem cell-mediated repair.

scholarly journals ZFP982 confers mouse embryonic stem cell characteristics by regulating expression of Nanog, Zfp42 and Dppa3

2020 ◽  
Author(s):  
Fariba Dehghanian ◽  
Patrick Piero Bovio ◽  
Zohreh Hojati ◽  
Tanja Vogel
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Embryonic Stem Cells ◽  
Neural Differentiation ◽  
Marker Gene ◽  
Embryonic Stem ◽  
Mouse Embryonic Stem Cells ◽  
Stem Cell Marker ◽  
Marker Genes ◽  
List Type

AbstractWe here used multi-omics analyses to identify and characterize zinc finger protein 982 (Zfp982) that confers stemness characteristics by regulating expression of Nanog, Zfp42 and Dppa3 in mouse embryonic stem cells (mESC). Network-based expression analyses comparing the transcriptional profiles of mESC and differentiated cells revealed high expression of Zfp982 in stem cells. Moreover, Zfp982 showed transcriptional overlap with Yap1, the major co-activator of the Hippo pathway. Quantitative proteomics and co-immunoprecipitation revealed interaction of ZFP982 with YAP1. ZFP982 used a GCAGAGKC motif to bind to chromatin, for example near the stemness conferring genes Nanog, Zfp42 and Dppa3 as shown by ChIP-seq. Loss-of-function experiments in mESC established that expression of Zfp982 is necessary to maintain stem cell characteristics. Zfp982 expression decreased with progressive differentiation, and knockdown of Zfp982 resulted in neural differentiation of mESC. ZFP982 localized to the nucleus in mESC and translocated to the cytoplasm upon neuronal differentiation. Similarly, YAP1 localized to the cytoplasm upon differentiation, but in mESC YAP1 was present in the nucleus and cytoplasm.Graphical AbstractZFP982 is a regulator of stemness of mouse embryonic stem cells and acts as transcription factor by activating expression of stem cell genes including Nanog, Dppa3 and Zfp42.HighlightsZfp982 is a new mouse stem cell defining marker gene.Zfp982 is co-expressed with Yap1 and stem cell marker genes in mESC.ZFP982 binds to DNA and induces expression of master genes of stemness in mESC.Expression of Zfp982 gene prevents neural differentiation and maintains stem cell characteristics.ZFP982 and YAP1 interact in mESC and translocate to the cytoplasm upon neural differentiation.

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