scholarly journals Activation of Sonic hedgehog signaling in neural progenitor cells promotes glioma development in the zebrafish optic pathway

Oncogenesis ◽  
2014 ◽  
Vol 3 (3) ◽  
pp. e96-e96 ◽  
Author(s):  
B Ju ◽  
W Chen ◽  
J M Spitsbergen ◽  
J Lu ◽  
P Vogel ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Sonic Hedgehog ◽  
Hedgehog Signaling ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Optic Pathway ◽  
Sonic Hedgehog Signaling

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.

Neuroprotective properties of cultured neural progenitor cells are associated with the production of sonic hedgehog

Neuroscience ◽  
2005 ◽  
Vol 131 (4) ◽  
pp. 899-916 ◽  
Author(s):  
V.F. Rafuse ◽  
P. Soundararajan ◽  
C. Leopold ◽  
H.A. Robertson
Keyword(s):  
Progenitor Cells ◽  
Sonic Hedgehog ◽  
Neural Progenitor Cells ◽  
Neural Progenitor

scholarly journals Sonic Hedgehog and BMP2 Exert Opposing Actions on Proliferation and Differentiation of Embryonic Neural Progenitor Cells

1999 ◽  
Vol 215 (1) ◽  
pp. 118-129 ◽  
Author(s):  
Gaofa Zhu ◽  
Mark F. Mehler ◽  
Jie Zhao ◽  
Shau Yu Yung ◽  
John A. Kessler
Keyword(s):  
Progenitor Cells ◽  
Sonic Hedgehog ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Proliferation And Differentiation

scholarly journals A subpopulation of astrocyte progenitors defined by Sonic hedgehog signaling

2022 ◽  
Vol 17 (1) ◽  
Author(s):  
Ellen C. Gingrich ◽  
Kendra Case ◽  
A. Denise R. Garcia
Keyword(s):  
Progenitor Cells ◽  
Sonic Hedgehog ◽  
Hedgehog Signaling ◽  
Adult Brain ◽  
Substantial Contribution ◽  
Molecular Signaling ◽  
Sonic Hedgehog Signaling ◽  
Independent Manner ◽  
Shh Signaling ◽  
Cortical Astrocyte

Abstract Background The molecular signaling pathway, Sonic hedgehog (Shh), is critical for the proper development of the central nervous system. The requirement for Shh signaling in neuronal and oligodendrocyte development in the developing embryo are well established. However, Shh activity is found in discrete subpopulations of astrocytes in the postnatal and adult brain. Whether Shh signaling plays a role in astrocyte development is not well understood. Methods Here, we use a genetic inducible fate mapping approach to mark and follow a population of glial progenitor cells expressing the Shh target gene, Gli1, in the neonatal and postnatal brain. Results In the neonatal brain, Gli1-expressing cells are found in the dorsolateral corner of the subventricular zone (SVZ), a germinal zone harboring astrocyte progenitor cells. Our data show that these cells give rise to half of the cortical astrocyte population, demonstrating their substantial contribution to the cellular composition of the cortex. Further, these data suggest that the cortex harbors astrocytes from different lineages. Gli1 lineage astrocytes are distributed across all cortical layers, positioning them for broad influence over cortical circuits. Finally, we show that Shh activity recurs in mature astrocytes in a lineage-independent manner, suggesting cell-type dependent roles of the pathway in driving astrocyte development and function. Conclusion These data identify a novel role for Shh signaling in cortical astrocyte development and support a growing body of evidence pointing to astrocyte heterogeneity.

scholarly journals Erratum: Mitogenic Sonic hedgehog signaling drives E2F1-dependent lipogenesis in progenitor cells and medulloblastoma

Oncogene ◽  
2011 ◽  
Vol 30 (4) ◽  
pp. 504-504 ◽  
Author(s):  
B Bhatia ◽  
M Hsieh ◽  
A M Kenney ◽  
Z Nahlé
Keyword(s):  
Progenitor Cells ◽  
Sonic Hedgehog ◽  
Hedgehog Signaling ◽  
Sonic Hedgehog Signaling

Abstract 3139: The microRNA 17-92 Cluster Mediates Sonic Hedgehog-driven Neurogenesis In Ischemic Neural Progenitor Cells

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Xianshuang Liu ◽  
Michael Chopp ◽  
Tao Tang ◽  
Haifa Kassis ◽  
Jennifer Xu ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Sonic Hedgehog ◽  
Functional Role ◽  
Neural Progenitor Cells ◽  
Neural Progenitor ◽  
Control Group ◽  
Western Blots ◽  
Shh Pathway ◽  
Empty Vector

Background: The Sonic hedgehog (Shh) pathway regulates stroke-induced neurogenesis. The present study investigated the functional role of the microRNA 17-92 (miR17-92) cluster in this process. Methods and Results: Analysis of miRNA microarray and real-time RT-PCR revealed that stroke substantially increased levels of individual members of the miR17-92 cluster: miR-18a (1.8±0.3), miR-19a (2.5±0.4), and miR-92a (1.9±0.3) expression in neural progenitor cells (NPCs) harvested from the subventricular zone (SVZ) of ischemic rats (n=6). Overexpression of the miR17-92 cluster in cultured NPCs significantly increased NPC proliferation measured by the number of BrdU positive cells (52±4% vs 28±2% in empty vector, n=3/group, p<0.05). Concurrently, overexpression of the miR17-92 cluster reduced PTEN (phosphatase and tensin homolog), a target of the miR17-92 cluster, protein levels by 70% compared to levels in NPCs transfected with an empty vector. PTEN suppresses cell proliferation. These data suggest that the stroke-upregulated miR17-92 cluster enhances NPC proliferation via downregulation of PTEN. To examine whether Shh regulates miR17-92 cluster expression, NPCs were incubated with recombinant human Shh (rhShh, 100ng/ml). We found that rhShh significantly (p<0.05) increased levels of individual members of the miR17-92 cluster: miR-18a (2.1±0.1), miR-19a (1.3±0.7), miR-19b (1.5±0.6) and miR-92a (1.9±0.8). Blockage of a Shh receptor Smo with cyclopamine suppressed rhShh-increased levels of miR-18a (0.9±0.08), miR-19a (0.7±0.01), miR-19b (0.6±0.05) and miR-92a (0.8±0.04). Attenuation of endogenous Shh in NPCs with siRNA also substantially decreased levels of miR-18a (0.6±0.1), miR-19a (0.4±0.05) and miR-92a (0.6±0.1) compared with levels in NPCs transfected with scrambled siRNA (1.0±0.2, n=3), indicating that Shh regulates miR17-92 expression. MYC is a downstream target of Shh. Western blots showed that stroke increased the protein level of N-MYC 1.8 fold in SVZ tissues and incubation of NPCs with rhShh elevated N-MYC levels by 1.8 fold, which was abrogated by cyclopamine (1.3 fold). N-MYC transduction resulted in significant increases in expression of the primary miR17-92 cluster (2.1±0.3 vs 1.0±0.2 in control group, n=3, p<0.05). These data suggest that the Shh pathway recruits N-MYC to regulate miR17-92 cluster expression in NPCs. Conclusion: Our data suggest a functional role of the miR17-92 cluster in mediating stroke-induced neurogenesis by the SHH/MYC signaling pathway, which provides new insight into molecular mechanisms of stroke-induced neurogenesis.

Sign in / Sign up

Export Citation Format

Share Document