scholarly journals Epigenetic mechanisms regulating fate specification of neural stem cells

2008 ◽  
Vol 363 (1500) ◽  
pp. 2099-2109 ◽  
Author(s):  
Masakazu Namihira ◽  
Jun Kohyama ◽  
Masahiko Abematsu ◽  
Kinichi Nakashima
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Epigenetic Modification ◽  
Rna Expression ◽  
Epigenetic Mechanisms ◽  
Epigenetic Alterations ◽  
Fate Specification ◽  
Neural Fate ◽  
Non Coding Rna ◽  
Dynamic Interplay

Neural stem cells (NSCs) possess the ability to self-renew and to differentiate along neuronal and glial lineages. These processes are defined by the dynamic interplay between extracellular cues including cytokine signalling and intracellular programmes such as epigenetic modification. There is increasing evidence that epigenetic mechanisms involving, for example, changes in DNA methylation, histone modification and non-coding RNA expression are closely associated with fate specification of NSCs. These epigenetic alterations could provide coordinated systems for regulating gene expression at each step of neural cell differentiation. Here we review the roles of epigenetics in neural fate specification in the mammalian central nervous system.

scholarly journals Neural Induction, Neural Fate Stabilization, and Neural Stem Cells

2002 ◽  
Vol 2 ◽  
pp. 1147-1166 ◽  
Author(s):  
Sally A. Moody ◽  
Hyun-Soo Je
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Neural Stem Cells ◽  
Neural Development ◽  
Current Knowledge ◽  
Embryonic Stem ◽  
Neural Induction ◽  
Neural Plate ◽  
Natural Rate ◽  
Neural Fate

The promise of stem cell therapy is expected to greatly benefit the treatment of neurodegenerative diseases. An underlying biological reason for the progressive functional losses associated with these diseases is the extremely low natural rate of self-repair in the nervous system. Although the mature CNS harbors a limited number of self-renewing stem cells, these make a significant contribution to only a few areas of brain. Therefore, it is particularly important to understand how to manipulate embryonic stem cells and adult neural stem cells so their descendants can repopulate and functionally repair damaged brain regions. A large knowledge base has been gathered about the normal processes of neural development. The time has come for this information to be applied to the problems of obtaining sufficient, neurally committed stem cells for clinical use. In this article we review the process of neural induction, by which the embryonic ectodermal cells are directed to form the neural plate, and the process of neural�fate stabilization, by which neural plate cells expand in number and consolidate their neural fate. We will present the current knowledge of the transcription factors and signaling molecules that are known to be involved in these processes. We will discuss how these factors may be relevant to manipulating embryonic stem cells to express a neural fate and to produce large numbers of neurally committed, yet undifferentiated, stem cells for transplantation therapies.

scholarly journals Identification of Qk as a Glial Precursor Cell Marker that Governs the Fate Specification of Neural Stem Cells to a Glial Cell Lineage

2020 ◽  
Vol 15 (4) ◽  
pp. 883-897
Author(s):  
Akihide Takeuchi ◽  
Yuji Takahashi ◽  
Kei Iida ◽  
Motoyasu Hosokawa ◽  
Koichiro Irie ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Glial Cell ◽  
Cell Lineage ◽  
Precursor Cell ◽  
Cell Marker ◽  
Fate Specification ◽  
Glial Precursor

scholarly journals Circular RNA expression profiles during the differentiation of mouse neural stem cells

2018 ◽  
Vol 12 (S8) ◽  
Author(s):  
Qichang Yang ◽  
Jing Wu ◽  
Jian Zhao ◽  
Tianyi Xu ◽  
Zhongming Zhao ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Expression Profiles ◽  
Circular Rna ◽  
Rna Expression

scholarly journals Direct Neural Fate Specification from Embryonic Stem Cells

Neuron ◽  
2001 ◽  
Vol 30 (1) ◽  
pp. 65-78 ◽  
Author(s):  
Vincent Tropepe ◽  
Seiji Hitoshi ◽  
Christian Sirard ◽  
Tak W Mak ◽  
Janet Rossant ◽  
...  
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Fate Specification ◽  
Neural Fate

scholarly journals Transcriptional factor FoxM1-activated microRNA-335-3p maintains the self-renewal of neural stem cells by inhibiting p53 signaling pathway via Fmr1

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jiaoying Jia ◽  
Yan Cui ◽  
Zhigang Tan ◽  
Min Liu ◽  
Yugang Jiang
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Signaling Pathway ◽  
Neurological Diseases ◽  
The Self ◽  
Self Renewal ◽  
P53 Signaling ◽  
Non Coding Rna ◽  
Fetal Rats ◽  
P53 Signaling Pathway

Abstract Background New mechanistic insights into the self-renewal ability and multipotent properties of neural stem cells (NSCs) are currently under active investigation for potential use in the treatment of neurological diseases. In this study, NSCs were isolated from the forebrain of fetal rats and cultured to induce NSC differentiation, which was associated with low expression of the non-coding RNA microRNA-335-3p (miR-335-3p). Methods Loss- and gain-of-function experiments were performed in NSCs after induction of differentiation. Results Overexpression of miR-335-3p or FoxM1 and inhibition of the Fmr1 or p53 signaling pathways facilitated neurosphere formation, enhanced proliferation and cell cycle entry of NSCs, but restricted NSC differentiation. Mechanistically, FoxM1 positively regulated miR-335-3p by binding to its promoter region, while miR-335-3p targeted and negatively regulated Fmr1. Additionally, the promotive effect of miR-335-3p on NSC self-renewal occurred via p53 signaling pathway inactivation. Conclusion Taken together, miR-335-3p activated by FoxM1 could suppress NSC differentiation and promote NSC self-renewal by inactivating the p53 signaling pathway via Fmr1.

scholarly journals Effects of Caloric Restriction on the Epigenetic Landscape of Hematopoietic Stem Cells

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 512-512
Author(s):  
Isabel Beerman
Keyword(s):  
Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Caloric Restriction ◽  
Adult Stem Cells ◽  
Epigenetic Modification ◽  
Functional Decline ◽  
Epigenetic Alterations ◽  
Hematopoietic Stem ◽  
Aged Mice ◽  
Ad Libitum

Abstract During aging, alterations of hematopoietic stem cells are associated with functional decline of the blood system. Caloric restriction (CR) interventions have been reported to improve adult stem cells in other tissue types during aging so we sought to evaluate the effects of CR on the aged HSC compartment. We find significant epigenetic alterations in HSCs isolated from aged mice after life-long CR compared to ad libitum fed aged mice. We further evaluated the epigenetic landscapes and functional potential of aged HSCs shortly after allowing life-long CR mice access to ad libitum food. We uncover epigenetic modification associated with functional alterations of the HSCs, defining potential mechanisms by which restrictions in food consumption affect the aging hematopoietic compartment.

Fate Specification of Neural Stem Cells

2011 ◽  
pp. 87-107 ◽  
Author(s):  
Masakazu Namihira ◽  
Kinichi Nakashima
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Fate Specification

Epigenetic Mechanisms and the Risk for PTSD

2018 ◽  
Author(s):  
Michael J. Meaney ◽  
Rachel Yehuda
Keyword(s):  
Parental Stress ◽  
Epigenetic Modification ◽  
Childhood Adversity ◽  
Epigenetic Mechanisms ◽  
Epigenetic Alterations ◽  
Ptsd Symptoms ◽  
Post Traumatic Stress ◽  
Increased Risk ◽  
Post Traumatic ◽  
Exposure To Trauma

This chapter discusses the epigenetic mechanisms involved in individual variation in and persistence of post-traumatic stress disorder (PTSD). Such mechanisms make it possible to trace vulnerability for PTSD to effects that predate development of PTSD. While some may be genetic in origin, others may involve parental stress occurring pre-conception, in utero changes in the maternal environment contributing to developmental programming, and childhood adversity, resulting in modifications of genes’ contribution to PTSD risk. The chapter discusses epigenetic alterations implicated in hypothalamic–pituitary–adrenal (HPA) function in PTSD that mark increased risk. Unlike the transient alterations in neural, endocrine, or immunological signals that follow exposure to trauma, certain epigenetic markers can be chemically stable over extended periods and can serve as a basis for understanding the persistence of PTSD symptoms. The chapter concludes with a discussion of how epigenetic modification may offer insights into future treatments for PTSD.

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