Effect of nitric oxide on the proliferation and differentiation of neural precursor cells derived from embryonic rat spinal cord

2009 ◽  
Author(s):  
Xiaoying Yang
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Rat Spinal Cord ◽  
Proliferation And Differentiation

Endogenous stem cell proliferation induced by intravenous hedgehog agonist administration after contusion in the adult rat spinal cord

2009 ◽  
Vol 10 (2) ◽  
pp. 171-176 ◽  
Author(s):  
Nicholas C. Bambakidis ◽  
Eric M. Horn ◽  
Peter Nakaji ◽  
Nicholas Theodore ◽  
Elizabeth Bless ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Intravenous Administration ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Rat Spinal Cord ◽  
Adult Rats ◽  
Significant Difference ◽  
Cord Injury

Object Sonic hedgehog (Shh) is a glycoprotein molecule that upregulates the transcription factor Gli1. The Shh protein plays a critical role in the proliferation of endogenous neural precursor cells when directly injected into the spinal cord after a spinal cord injury in adult rodents. Small-molecule agonists of the hedgehog (Hh) pathway were used in an attempt to reproduce these findings through intravenous administration. Methods The expression of Gli1 was measured in rat spinal cord after the intravenous administration of an Hh agonist. Ten adult rats received a moderate contusion and were treated with either an Hh agonist (10 mg/kg, intravenously) or vehicle (5 rodents per group) 1 hour and 4 days after injury. The rats were killed 5 days postinjury. Tissue samples were immediately placed in fixative. Samples were immunohistochemically stained for neural precursor cells, and these cells were counted. Results Systemic dosing with an Hh agonist significantly upregulated Gli1 expression in the spinal cord (p < 0.005). After spinal contusion, animals treated with the Hh agonist had significantly more nestin-positive neural precursor cells around the rim of the lesion cavity than in vehicle-treated controls (means ± SDs, 46.9 ± 12.9 vs 20.9 ± 8.3 cells/hpf, respectively, p < 0.005). There was no significant difference in the area of white matter injury between the groups. Conclusions An intravenous Hh agonist at doses that upregulate spinal cord Gli1 transcription also increases the population of neural precursor cells after spinal cord injury in adult rats. These data support previous findings based on injections of Shh protein directly into the spinal cord.

Electrophysiological Properties of Mitogen-Expanded Adult Rat Spinal Cord and Subventricular Zone Neural Precursor Cells

1999 ◽  
Vol 158 (1) ◽  
pp. 143-154 ◽  
Author(s):  
Rong-Huan Liu ◽  
Dante J. Morassutti ◽  
Scott R. Whittemore ◽  
Jeffrey S. Sosnowski ◽  
David S.K. Magnuson
Keyword(s):  
Spinal Cord ◽  
Subventricular Zone ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Rat Spinal Cord ◽  
Electrophysiological Properties ◽  
Adult Rat ◽  
Adult Rat Spinal Cord

Human neural precursor cells continue to proliferate and exhibit low cell death after transplantation to the injured rat spinal cord

2009 ◽  
Vol 1278 ◽  
pp. 15-26 ◽  
Author(s):  
Mia Emgård ◽  
Lena Holmberg ◽  
Eva-Britt Samuelsson ◽  
Ben A. Bahr ◽  
Scott Falci ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Rat Spinal Cord

scholarly journals Three Growth Factors Induce Proliferation and Differentiation of Neural Precursor Cells In Vitro and Support Cell-Transplantation after Spinal Cord Injury In Vivo

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Alexander Younsi ◽  
Guoli Zheng ◽  
Moritz Scherer ◽  
Lennart Riemann ◽  
Hao Zhang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Growth Factors ◽  
Financial Burden ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Cord Injury ◽  
Proliferation And Differentiation

Stem cell therapy with neural precursor cells (NPCs) has the potential to improve neuroregeneration after spinal cord injury (SCI). Unfortunately, survival and differentiation of transplanted NPCs in the injured spinal cord remains low. Growth factors have been successfully used to improve NPC transplantation in animal models, but their extensive application is associated with a relevant financial burden and might hinder translation of findings into the clinical practice. In our current study, we assessed the potential of a reduced number of growth factors in different combinations and concentrations to increase proliferation and differentiation of NPCs in vitro. After identifying a “cocktail” (EGF, bFGF, and PDGF-AA) that directed cell fate towards the oligodendroglial and neuronal lineage while reducing astrocytic differentiation, we translated our findings into an in vivo model of cervical clip contusion/compression SCI at the C6 level in immunosuppressed Wistar rats, combining NPC transplantation and intrathecal administration of the growth factors 10 days after injury. Eight weeks after SCI, we could observe surviving NPCs in the injured animals that had mostly differentiated into oligodendrocytes and oligodendrocytic precursors. Moreover, “Stride length” and “Average Speed” in the CatWalk gait analysis were significantly improved 8 weeks after SCI, representing beneficial effects on the functional recovery with NPC transplantation and the administration of the three growth factors. Nevertheless, no effects on the BBB scores could be observed over the course of the experiment and regeneration of descending tracts as well as posttraumatic myelination remained unchanged. However, reactive astrogliosis, as well as posttraumatic inflammation and apoptosis was significantly reduced after NPC transplantation and GF administration. Our data suggest that NPC transplantation is feasible with the use of only EGF, bFGF, and PDGF-AA as supporting growth factors.

Transplantation of Clonal Neural Precursor Cells Derived from Adult Human Brain Establishes Functional Peripheral Myelin in the Rat Spinal Cord

2001 ◽  
Vol 167 (1) ◽  
pp. 27-39 ◽  
Author(s):  
Yukinori Akiyama ◽  
Osamu Honmou ◽  
Takaaki Kato ◽  
Teiji Uede ◽  
Kazuo Hashi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Human Brain ◽  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Rat Spinal Cord ◽  
Adult Human Brain ◽  
Adult Human

scholarly journals MRG15, a component of HAT and HDAC complexes, is essential for proliferation and differentiation of neural precursor cells

2009 ◽  
Vol 87 (7) ◽  
pp. 1522-1531 ◽  
Author(s):  
Meizhen Chen ◽  
Masumi Takano-Maruyama ◽  
Olivia M. Pereira-Smith ◽  
Gary O. Gaufo ◽  
Kaoru Tominaga
Keyword(s):  
Precursor Cells ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Proliferation And Differentiation

scholarly journals Stabilized β-Catenin Functions through TCF/LEF Proteins and the Notch/RBP-Jκ Complex To Promote Proliferation and Suppress Differentiation of Neural Precursor Cells

2008 ◽  
Vol 28 (24) ◽  
pp. 7427-7441 ◽  
Author(s):  
Takeshi Shimizu ◽  
Tetsushi Kagawa ◽  
Toshihiro Inoue ◽  
Aya Nonaka ◽  
Shinji Takada ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Neuronal Differentiation ◽  
Glycogen Synthase ◽  
Precursor Cells ◽  
Precursor Cell ◽  
Neural Precursor Cells ◽  
Neural Precursor ◽  
Self Renewal ◽  
Fgf Receptor ◽  
Proliferation And Differentiation

ABSTRACT The proliferation and differentiation of neural precursor cells are mutually exclusive during brain development. Despite its importance for precursor cell self renewal, the molecular linkage between these two events has remained unclear. Fibroblast growth factor 2 (FGF2) promotes neural precursor cell proliferation and concurrently inhibits their differentiation, suggesting a cross talk between proliferation and differentiation signaling pathways downstream of the FGF receptor. We demonstrate that FGF2 signaling through phosphatidylinositol 3 kinase activation inactivates glycogen synthase kinase 3β (GSK3β) and leads to the accumulation of β-catenin in a manner different from that in the Wnt canonical pathway. The nuclear accumulated β-catenin leads to cell proliferation by activating LEF/TCF transcription factors and concurrently inhibits neuronal differentiation by potentiating the Notch1-RBP-Jκ signaling pathway. β-Catenin and the Notch1 intracellular domain form a molecular complex with the promoter region of the antineurogenic hes1 gene, allowing its expression. This signaling interplay is especially essential for neural stem cell maintenance, since the misexpression of dominant-active GSK3β completely inhibits the self renewal of neurosphere-forming stem cells and prompts their neuronal differentiation. Thus, the GSK3β/β-catenin signaling axis regulated by FGF and Wnt signals plays a pivotal role in the maintenance of neural stem/precursor cells by linking the cell proliferation to the inhibition of differentiation.

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