Specific Roles of JAKs and STAT3 in Functions of Neural Stem Cells and Committed Neuronal Progenitors during Ethanol-Induced Neurodegeneration

2020 ◽  
Vol 168 (3) ◽  
pp. 356-360 ◽  
Author(s):  
G. N. Zyuz’kov ◽  
L. A. Miroshnichenko ◽  
T. Yu. Polyakova ◽  
L. A. Stavrova ◽  
E. V. Simanina ◽  
...  
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Neuronal Progenitors

scholarly journals Erythropoietin Regulates theIn VitroandIn VivoProduction of Neuronal Progenitors by Mammalian Forebrain Neural Stem Cells

2001 ◽  
Vol 21 (24) ◽  
pp. 9733-9743 ◽  
Author(s):  
Tetsuro Shingo ◽  
S. Todd Sorokan ◽  
Takuya Shimazaki ◽  
Samuel Weiss
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Neuronal Progenitors

scholarly journals Understanding microcephaly through the study of centrosome regulation in Drosophila neural stem cells

2020 ◽  
Vol 48 (5) ◽  
pp. 2101-2115
Author(s):  
Beverly V. Robinson ◽  
Victor Faundez ◽  
Dorothy A. Lerit
Keyword(s):  
Stem Cells ◽  
Drosophila Melanogaster ◽  
Cell Division ◽  
Virus Infection ◽  
Neural Stem Cells ◽  
Head Circumference ◽  
Zika Virus ◽  
Asymmetric Cell Division ◽  
Significant Proportion ◽  
Neuronal Progenitors

Microcephaly is a rare, yet devastating, neurodevelopmental condition caused by genetic or environmental insults, such as the Zika virus infection. Microcephaly manifests with a severely reduced head circumference. Among the known heritable microcephaly genes, a significant proportion are annotated with centrosome-related ontologies. Centrosomes are microtubule-organizing centers, and they play fundamental roles in the proliferation of the neuronal progenitors, the neural stem cells (NSCs), which undergo repeated rounds of asymmetric cell division to drive neurogenesis and brain development. Many of the genes, pathways, and developmental paradigms that dictate NSC development in humans are conserved in Drosophila melanogaster. As such, studies of Drosophila NSCs lend invaluable insights into centrosome function within NSCs and help inform the pathophysiology of human microcephaly. This mini-review will briefly survey causative links between deregulated centrosome functions and microcephaly with particular emphasis on insights learned from Drosophila NSCs.

scholarly journals p53 upregulated mediator of apoptosis (Puma) deficiency increases survival of adult neural stem cells generated physiologically in the hippocampus, but does not protect stem cells generated in surplus after an excitotoxic lesion

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Eva C. Bunk ◽  
Hans-Georg König ◽  
Jochen H.M. Prehn ◽  
Brian P. Kirby
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Apoptotic Cell ◽  
Mammalian Brain ◽  
Survival Times ◽  
Neuronal Progenitors ◽  
Proliferation And Differentiation ◽  
Immunofluorescence Labelling ◽  
Domain 3 ◽  
Excitotoxic Lesion

AbstractObjectivesNeurogenesis occurs in the mammalian brain throughout adulthood and increases in response to metabolic, toxic or traumatic insults. To remove potentially superfluous or unwanted neural stem cells/neuronal progenitors, their rate of proliferation and differentiation is fine-tuned against their rate of apoptosis. Apoptosis requires the transcriptional and posttranslational activation of Bcl-2-homolgy domain 3 (BH3)-only proteins. Previously, we demonstrated that the BH3-only protein p53-upregulated mediator of apoptosis (Puma) controls the physiological rate of apoptosis of neural precursor cells in the adult mouse hippocampus. Puma’s role in controlling a lesion-induced increase in neural stem cells is currently not known.MethodsWe employed a model of local, N-methyl-D-asparte (NMDA)-induced excitotoxic injury to the CA1 hippocampal subfield and immunofluorescence labelling to produce increased neural stem cell proliferation/ neurogenesis in the dentate gyrus at two survival times following the excitotoxic lesion.ResultsDeletion of puma failed to rescue any NMDA-induced increase in adult born cells as assessed by BrdU or Doublecortin labelling in the long-term. No difference in the proportion of BrdU/NeuN-positive cells comparing the different genotypes and treatments suggested that the phenotypic fate of the cells was preserved regardless of the genotype and the treatment.ConclusionsWhile neurogenesis is up-regulated in puma-deficient animals following NMDA-induced excitotoxicity to the hippocampal CA1 subfield, puma deficiency could not protect this surplus of newly generated cells from apoptotic cell death.

scholarly journals Neuregulin-1 increases the proliferation of neuronal progenitors from embryonic neural stem cells

2005 ◽  
Vol 283 (2) ◽  
pp. 437-445 ◽  
Author(s):  
Yun Liu ◽  
Byron D. Ford ◽  
Mary Anne Mann ◽  
Gerald D. Fischbach
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Neuregulin 1 ◽  
Neuronal Progenitors

scholarly journals Irx3 and Irx5 - Novel Regulatory Factors of Postnatal Hypothalamic Neurogenesis

2021 ◽  
Vol 15 ◽  
Author(s):  
Zhengchao Dou ◽  
Joe Eun Son ◽  
Chi-chung Hui
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
Energy Homeostasis ◽  
Adult Mouse ◽  
Radial Glia ◽  
Current Knowledge ◽  
Cell Types ◽  
Neuronal Populations ◽  
Neuronal Progenitors ◽  
Physiological Processes

The hypothalamus is a brain region that exhibits highly conserved anatomy across vertebrate species and functions as a central regulatory hub for many physiological processes such as energy homeostasis and circadian rhythm. Neurons in the arcuate nucleus of the hypothalamus are largely responsible for sensing of peripheral signals such as leptin and insulin, and are critical for the regulation of food intake and energy expenditure. While these neurons are mainly born during embryogenesis, accumulating evidence have demonstrated that neurogenesis also occurs in postnatal-adult mouse hypothalamus, particularly in the first two postnatal weeks. This second wave of active neurogenesis contributes to the remodeling of hypothalamic neuronal populations and regulation of energy homeostasis including hypothalamic leptin sensing. Radial glia cell types, such as tanycytes, are known to act as neuronal progenitors in the postnatal mouse hypothalamus. Our recent study unveiled a previously unreported radial glia-like neural stem cell (RGL-NSC) population that actively contributes to neurogenesis in the postnatal mouse hypothalamus. We also identified Irx3 and Irx5, which encode Iroquois homeodomain-containing transcription factors, as genetic determinants regulating the neurogenic property of these RGL-NSCs. These findings are significant as IRX3 and IRX5 have been implicated in FTO-associated obesity in humans, illustrating the importance of postnatal hypothalamic neurogenesis in energy homeostasis and obesity. In this review, we summarize current knowledge regarding postnatal-adult hypothalamic neurogenesis and highlight recent findings on the radial glia-like cells that contribute to the remodeling of postnatal mouse hypothalamus. We will discuss characteristics of the RGL-NSCs and potential actions of Irx3 and Irx5 in the regulation of neural stem cells in the postnatal-adult mouse brain. Understanding the behavior and regulation of neural stem cells in the postnatal-adult hypothalamus will provide novel mechanistic insights in the control of hypothalamic remodeling and energy homeostasis.

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