scholarly journals Mifepristone-inducible transgene expression in neural progenitor cells in vitro and in vivo

Gene Therapy ◽  
2016 ◽  
Vol 23 (5) ◽  
pp. 424-437 ◽  
Author(s):  
B E Hjelm ◽  
C Grunseich ◽  
G Gowing ◽  
P Avalos ◽  
J Tian ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Transgene Expression ◽  
Neural Progenitor Cells ◽  
Neural Progenitor

scholarly journals SBE6: a novel long-range enhancer involved in driving sonic hedgehog expression in neural progenitor cells

Open Biology ◽  
2016 ◽  
Vol 6 (11) ◽  
pp. 160197 ◽  
Author(s):  
Nezha S. Benabdallah ◽  
Philippe Gautier ◽  
Betul Hekimoglu-Balkan ◽  
Laura A. Lettice ◽  
Shipra Bhatia ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Long Range ◽  
Sonic Hedgehog ◽  
Neural Progenitor Cells ◽  
Embryonic Stem ◽  
Regulatory Elements ◽  
Neural Progenitor ◽  
Chromatin Profiling

The expression of genes with key roles in development is under very tight spatial and temporal control, mediated by enhancers. A classic example of this is the sonic hedgehog gene ( Shh ), which plays a pivotal role in the proliferation, differentiation and survival of neural progenitor cells both in vivo and in vitro. Shh expression in the brain is tightly controlled by several known enhancers that have been identified through genetic, genomic and functional assays. Using chromatin profiling during the differentiation of embryonic stem cells to neural progenitor cells, here we report the identification of a novel long-range enhancer for Shh—Shh-brain-enhancer-6 (SBE6)—that is located 100 kb upstream of Shh and that is required for the proper induction of Shh expression during this differentiation programme. This element is capable of driving expression in the vertebrate brain. Our study illustrates how a chromatin-focused approach, coupled to in vivo testing, can be used to identify new cell-type specific cis -regulatory elements, and points to yet further complexity in the control of Shh expression during embryonic brain development.

CTN-986, a compound extracted from cottonseeds, increases cell proliferation in hippocampus in vivo and in cultured neural progenitor cells in vitro

2009 ◽  
Vol 607 (1-3) ◽  
pp. 110-113 ◽  
Author(s):  
Li-Ming Zhang ◽  
You-Zhi Zhang ◽  
Yan-Qin Liu ◽  
Ze-Hui Gong ◽  
Yi-Min Zhao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Neural Progenitor

Lithium selectively increases neuronal differentiation of hippocampal neural progenitor cells both in vitro and in vivo

2004 ◽  
Vol 89 (2) ◽  
pp. 324-336 ◽  
Author(s):  
Jin Seuk Kim ◽  
Mi-Yoon Chang ◽  
In Tag Yu ◽  
Ju Hee Kim ◽  
Sang-Hun Lee ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Neuronal Differentiation ◽  
Neural Progenitor Cells ◽  
Neural Progenitor

scholarly journals Efficient Transduction of Feline Neural Progenitor Cells for Delivery of Glial Cell Line-Derived Neurotrophic Factor Using a Feline Immunodeficiency Virus-Based Lentiviral Construct

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
X. Joann You ◽  
Ping Gu ◽  
Jinmei Wang ◽  
Tianran Song ◽  
Jing Yang ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Glial Cell ◽  
Neurotrophic Factor ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Degenerative Disease ◽  
Before And After ◽  
A Cell

Work has shown that stem cell transplantation can rescue or replace neurons in models of retinal degenerative disease. Neural progenitor cells (NPCs) modified to overexpress neurotrophic factors are one means of providing sustained delivery of therapeutic gene products in vivo. To develop a nonrodent animal model of this therapeutic strategy, we previously derived NPCs from the fetal cat brain (cNPCs). Here we use bicistronic feline lentiviral vectors to transduce cNPCs with glial cell-derived neurotrophic factor (GDNF) together with a GFP reporter gene. Transduction efficacy is assessed, together with transgene expression level and stability during induction of cellular differentiation, together with the influence of GDNF transduction on growth and gene expression profile. We show that GDNF overexpressing cNPCs expand in vitro, coexpress GFP, and secrete high levels of GDNF protein—before and after differentiation—all qualities advantageous for use as a cell-based approach in feline models of neural degenerative disease.

Oct-3/4 repression accelerates differentiation of neural progenitor cells in vitro and in vivo

2004 ◽  
Vol 132 (1) ◽  
pp. 18-30 ◽  
Author(s):  
Tomohiro Okuda ◽  
Kazuhiko Tagawa ◽  
Mei-Ling Qi ◽  
Masataka Hoshio ◽  
Hiroko Ueda ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Neural Progenitor

Abstract 141: The Microrna 17-92 Cluster in Neural Progenitor Cells is Required for Stroke-induced Neurogenesis and Gliogenesis

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Wanlong Pan ◽  
Xianshuang Liu ◽  
Xiaoming Zhang ◽  
Xinli Wang ◽  
Jiani Hu ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Molecular Mechanisms ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Artery Occlusion ◽  
Tamoxifen Treatment ◽  
Oligodendrocyte Progenitor Cells ◽  
Factor Inhibitor

Background: Molecular mechanisms underlying stroke-induced neurogenesis have not been fully investigated. The microRNA 17-92 cluster (miR17-92) regulates proliferation and differentiation of adult neural progenitor cells (NPCs). The present study investigated whether the miR17-92 cluster in NPCs is required for stroke-induced neurogenesis. Methods and Results: Mice with inducible and conditional knockdown of the miR17-92 cluster in nestin lineage NPCs (nestin-CreER T2 /miR17-92 -/- , 17-92-cKO, n=9) and wild-type litters (WT, n=9) were treated by tamoxifen. Administration of tamoxifen resulted in more than 60% reduction of individual members of the miR-17-92 cluster (miR-17: 1.0 vs 0.4; miR-19a: 1.0 vs 0.3; miR-19b: 1.0 vs 0.2; miR-20a: 1.0 vs 0.4; miR-92a: 1.0 vs 0.4 fold in WT, p<0.05) in NPCs localized to the subventricular zone (SVZ). Two days after termination of tamoxifen treatment, these mice were subjected to permanent right middle cerebral artery occlusion (MCAO) and sacrificed 28 days post-MCAo. Compared to WT mice, 17-92-cKO mice exhibited significant (p<0.05) reduction of proliferation of NPCs measured by the number of Ki67 + cells (226±43 vs 471±100 cells/mm 2 ) and the number of DCX + neuroblasts (11±2% vs 24±4% ) in the ischemic SVZ. Cultured NPCs harvested from ischemic cKO mice showed significant (p<0.05) reduction of BrdU + cells (37±2% vs 61±4% WT , n=3/group), Tuj1 + neuroblasts (5±0.2% vs 9±0.4% ), GFAP + cells (33±3% vs 53±2% ), and NG2 + oligodendrocyte progenitor cells (OPCs, 3±0.1% vs 5±0.5%). These in vivo and in vitro data indicate that reduction of the miR17-92 cluster suppresses stroke-induced neurogenesis and gliogenesis. Western blot analysis showed that miR17-92 cKO significantly (p<0.05) increased and reduced a cytoskeleton-associated protein, Enigma homolog1 (ENH1, 1.6 vs 1.0 fold), and its down-stream transcription factor, inhibitor of differentiation1 (ID1, 1.0 vs 0.6 fold), respectively. ENH1 is a putative target of the miR17-92 cluster. Conclusion: Our data indicate that the miR17-92 cluster in adult nestin lineage NPCs is required for stroke-induced neurongenesis and gliogenesis, and that the miR17-92 cluster possibly targets ENH1/ID1 signaling.

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