scholarly journals Exercise Increases Neural Stem Cell Number in a Growth Hormone-Dependent Manner, Augmenting the Regenerative Response in Aged Mice

Stem Cells ◽  
2009 ◽  
Vol 27 (8) ◽  
pp. 2044-2052 ◽  
Author(s):  
Daniel G. Blackmore ◽  
Mohammad G. Golmohammadi ◽  
Beatrice Large ◽  
Michael J. Waters ◽  
Rodney L. Rietze
Keyword(s):  
Growth Hormone ◽  
Stem Cell ◽  
Neural Stem Cell ◽  
Cell Number ◽  
Dependent Manner ◽  
Aged Mice ◽  
Regenerative Response

scholarly journals Roles for HIF-1α in neural stem cell function and the regenerative response to stroke

2012 ◽  
Vol 227 (2) ◽  
pp. 410-417 ◽  
Author(s):  
Lee Anna Cunningham ◽  
Kate Candelario ◽  
Lu Li
Keyword(s):  
Stem Cell ◽  
Neural Stem Cell ◽  
Cell Function ◽  
Regenerative Response

scholarly journals Neural stem cell conditioned medium alleviates Aβ25-35 damage to SH-SY5Y cells through the PCMT1/MST1 pathway

2020 ◽  
Author(s):  
Guoyong Jia ◽  
Hongna Yang ◽  
Zengyan Diao ◽  
Ying Liu ◽  
Congcong Sun
Keyword(s):  
Stem Cell ◽  
Cell Viability ◽  
Conditioned Medium ◽  
Neural Stem Cell ◽  
Inhibitory Effect ◽  
Complete Medium ◽  
Dependent Manner ◽  
Induced Apoptosis ◽  
Dose Dependent ◽  
Cell Conditioned Medium

Alzheimer’s disease (AD) is a progressive, neurodegenerative disease. Accumulating evidence suggests that protein isoaspartate methyltransferase 1 (PCMT1) is highly expressed in brain tissue (substantia nigra, blue plaque, paraventricular nucleus). In this study, we investigated the effect of neural stem cell conditioned medium alleviates Aβ25-35 damage to SH-SY5Y cells by PCMT1/MST1 pathway. Results demonstrated that Aβ25-35 significantly decreased the cell viability in time and dose dependent manner. However, Neural stem cell-complete medium (NSC-CPM) or NSC-CDM had inhibitory effect on toxicity when fibrillation of Aβ25-35 occurred in their presence and NSC-CDM had a better inhibitor result. An increase of the PCMT1 expression levels was found in Aβ25-35 + NSC-CDM group. sh-PCMT1 significantly reduced the PCMT1, the cell viability and inhibited the protective effect; induced apoptosis and increased the expression of p-MST1. Overexpression of PCMT1 group reversed the effect of Aβ25-35 inhibited the cell viability and Aβ25-35 induced the apoptosis. In conclusion, NSC-CDM corrects the damage of Aβ25-35 to cells by increasing PCMT1, reducing MST phosphorylation.

AMN107 Appears Equipotent and May Synergise with Imatinib at the CML Stem Cell Level through Interaction with ABCG2.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1080-1080 ◽  
Author(s):  
H. Jorgensen ◽  
E. Allan ◽  
N. Jordanides ◽  
A. Hamilton ◽  
J. Mountford ◽  
...  
Keyword(s):  
Stem Cells ◽  
Flow Cytometry ◽  
Stem Cell ◽  
Single Agent ◽  
Cell Number ◽  
Total Cell ◽  
Dependent Manner ◽  
Cell Level ◽  
Clinical Resistance

Abstract AMN107 (Novartis) is a novel Abl tyrosine kinase inhibitor specifically developed to be more selective for BcrAbl. AMN107 also maintains activity against the most common mutations associated with clinical resistance to imatinib mesylate (IM). In preclinical studies in cell lines and animal models, AMN107 was found to have greater potency than IM. By 3H-thymidine proliferation assays, the IC50 for AMN107 in K562 cells was 30 +/− 10nM compared with 600 +/− 60nM for IM. AMN107 and IM reduced K562 output cell number to 25% of input at 50 and 1000nM respectively, at 72h. These data are in keeping with the reported 20-fold increase in potency of AMN107 over IM. In addition, we have tested AMN107 for in vitro activity against primary CD34+Ph+ CML cells during 72h of culture in 5 growth factors. In CML cells (n=5), AMN107 and IM failed to reduce input cell number although the total cell output was restricted to 50% of PBS treated control at 2 +/− 1μM for AMN107 and to 31 +/− 7% of PBS treated control for 5μM IM suggesting the drugs were equipotent. The ability of the drugs to inhibit BcrAbl activity was then measured indirectly via the phosphorylation status of CrkL using a specific antiphospho-CrkL antibody and flow cytometry. Once again AMN107 and IM appeared equipotent in CML cells with 5μM of each compound leading to equal de-phosphorylation of CrkL. We next tested the efficacy of AMN107 as a single agent and in combination with IM against quiescent CML cells using in vitro dye (CFSE) tracking experiments. We evaluated by flow cytometry the proportion of input cells remaining alive, CD34+ and undivided (CFSEmax) or in first division. Compared to PBS treated control, 1.7, 2.5, 3.8 and 4.7-fold increases were found in the proportion of input CD34+ cells recovered in divisions 0 and 1 after 3 days exposure to 0.005, 0.05, 0.5 and 5μM AMN107, respectively. This was less accumulation than observed in the IM (5μM)-treated cells (11.0-fold). The combination of IM and AMN107, each at 5μM, was more effective in terms of total cell kill (54 and 74% fewer total cells remaining than with IM and AMN107 alone, respectively) and resulted in fewer viable cells recovered in divisions 0 and 1 than with either agent alone (for the combination, 1.9-fold on PBS treated recovery). We finally assessed the role of ABCG2 in modulating AMN107’s access to its intracellular BcrAbl target. We have previously shown ABCG2 to be over-expressed on CML stem cells and to interact with IM (Blood (2004); 104: 205a). We hypothesised that AMN107 and IM may co-operate as ABCG2 substrates or inhibitors to increase the intracellular levels of either or both drugs thus amplifying their efficacy against target protein specifically in CML stem cells. In competition assays with a known fluorescent substrate of ABCG2 (ie BODIPY-prazosin, BP), a specific inhibitor of the ABCG2 pump (fumitremorgin C, FTC) and an ABCG2 stably transfected AML cell line (AML6.2), the sample treated with BP plus FTC is taken to have greatest retention (100%). AMN107 inhibited efflux in a dose dependent manner to a maximum of 88% at 5μM, similarly to IM. Thus, AMN107 was equipotent with IM in primary CML stem cells in terms of restricting cell growth, inhibiting BcrAbl activity and interacting with ABCG2. However, AMN107 alone lead to less accumulation of quiescent CML cells in vitro as compared to IM, with the combination even more effective in this regard. The apparent co-operative effect of AMN107 and IM at the stem cell level would be predicted to improve clinical responses if tolerated in patients.

scholarly journals Soluble APP functions as a vascular niche signal that controls adult neural stem cell number

Development ◽  
2017 ◽  
Vol 144 (15) ◽  
pp. 2730-2736 ◽  
Author(s):  
Yuya Sato ◽  
Yutaka Uchida ◽  
Jingqiong Hu ◽  
Tracy L. Young-Pearse ◽  
Takako Niikura ◽  
...  
Keyword(s):  
Stem Cell ◽  
Neural Stem Cell ◽  
Cell Number ◽  
Adult Neural Stem Cell ◽  
Vascular Niche

YAP/TAZ enhance mammalian embryonic neural stem cell characteristics in a Tead-dependent manner

2015 ◽  
Vol 458 (1) ◽  
pp. 110-116 ◽  
Author(s):  
Dasol Han ◽  
Sung-Hyun Byun ◽  
Soojeong Park ◽  
Juwan Kim ◽  
Inhee Kim ◽  
...  
Keyword(s):  
Stem Cell ◽  
Neural Stem Cell ◽  
Dependent Manner ◽  
Embryonic Neural Stem Cell

Tramtrack controls glial number and identity in the Drosophila embryonic CNS

Development ◽  
2001 ◽  
Vol 128 (20) ◽  
pp. 4093-4101 ◽  
Author(s):  
Paul Badenhorst
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Neural Stem Cell ◽  
System Analysis ◽  
Cell Formation ◽  
S Phase ◽  
Dependent Manner ◽  
Multipotent Stem Cells ◽  
Protein Levels ◽  
Cycle Dependent

Neurons and glia are often derived from common multipotent stem cells. In Drosophila, neural identity appears to be the default fate of these precursors. Stem cells that generate either neurons or glia transiently express neural stem cell-specific markers. Further development as glia requires the activation of glial-specific regulators. However, this must be accompanied by simultaneous repression of the alternate neural fate. I show that the Drosophila transcriptional repressor Tramtrack is a key repressor of neuronal fates. It is expressed at high levels in all mature glia of the embryonic central nervous system. Analysis of the temporal profile of Tramtrack expression in glia shows that it follows that of existing glial markers. When expressed ectopically before neural stem cell formation, Tramtrack represses the neural stem cell-specific genes asense and deadpan. Surprisingly, Tramtrack protein levels oscillate in a cell cycle-dependent manner in proliferating glia, with expression dropping before replication, but re-initiating after S phase. Overexpression of Tramtrack blocks glial development by inhibiting S-phase and repressing expression of the S-phase cyclin, cyclin E. Conversely, in tramtrack mutant embryos, glia are disrupted and undergo additional rounds of replication. I propose that Tramtrack ensures stable mature glial identity by both repressing neuroblast-specific genes and controlling glial cell proliferation.

The Novel Free Radical Scavenger, Edaravone, Increases Neural Stem Cell Number Around the Area of Damage Following Rat Traumatic Brain Injury

2009 ◽  
Vol 16 (4) ◽  
pp. 378-389 ◽  
Author(s):  
Tatsuki Itoh ◽  
Takao Satou ◽  
Shozo Nishida ◽  
Masahiro Tsubaki ◽  
Shigeo Hashimoto ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Stem Cell ◽  
Free Radical ◽  
Brain Injury ◽  
Neural Stem Cell ◽  
Cell Number ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
The Novel

scholarly journals miR-17~92 exerts stage-specific effects in adult V-SVZ neural stem cell lineages

2021 ◽  
Author(s):  
Fabrizio Favaloro ◽  
Annina DeLeo ◽  
Ana Delgado ◽  
Fiona Doetsch
Keyword(s):  
Stem Cell ◽  
Neural Stem Cell ◽  
Oligodendrocyte Progenitor Cells ◽  
Dependent Manner ◽  
Cell Lineages ◽  
Conditional Deletion ◽  
Specific Effects ◽  
Cell Type Specific

In the adult mouse brain, neural stem cells (NSCs) in the ventricular-subventricular zone (V-SVZ) generate neurons and glia throughout life. microRNAs are important regulators of cell states, frequently acting in a stage- or context-dependent manner. Here, miRNA profiling of FACS-purified populations identified miR-17~92 as highly upregulated in activated NSCs and transit amplifying cells (TACs) in comparison to quiescent NSCs. Conditional deletion of miR-17~92 in NSCs reduced stem cell proliferation both in vitro and in vivo. In contrast, in TACs, miR-17~92 deletion caused a selective shift from neurogenic DLX2+ TACs towards oligodendrogenic OLIG2+ TACs, resulting in increased oligodendrogenesis to the corpus callosum. miR-17~92 deletion also decreased proliferation and maturation of intraventricular oligodendrocyte progenitor cells. Together, these findings reveal stage- and cell-type- specific functions of the miR-17~92 cluster within adult V-SVZ neural stem cell lineages.

Growth hormone and prolactin regulate human neural stem cell regenerative activity

Neuroscience ◽  
2011 ◽  
Vol 190 ◽  
pp. 409-427 ◽  
Author(s):  
P. Pathipati ◽  
T. Gorba ◽  
A. Scheepens ◽  
V. Goffin ◽  
Y. Sun ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Stem Cell ◽  
Neural Stem Cell ◽  
Human Neural Stem Cell ◽  
Regenerative Activity
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