scholarly journals Fishing for Contact: Modeling Perivascular Glioma Invasion in the Zebrafish Brain

2020 ◽  
Author(s):  
Robyn A. Umans ◽  
Mattie ten Kate ◽  
Carolyn Pollock ◽  
Harald Sontheimer
Keyword(s):  
Glioma Invasion ◽  
Contact Modeling ◽  
Zebrafish Brain

scholarly journals Fishing for contact: Modeling perivascular glioma invasion in the zebrafish brain

2020 ◽  
Author(s):  
Robyn A. Umans ◽  
Mattie ten Kate ◽  
Carolyn Pollock ◽  
Harald Sontheimer
Keyword(s):  
Blood Vessels ◽  
Cancer Biology ◽  
Standard Of Care ◽  
Model System ◽  
Adherent Cell ◽  
Tumor Vessel ◽  
Current Standard ◽  
Glioma Invasion ◽  
Tumor Cell Migration ◽  
Zebrafish Brain

AbstractGlioblastoma multiforme (GBM) is a highly invasive, central nervous system (CNS) cancer for which there is no a cure. Invading tumor cells evade treatment, limiting the efficacy of the current standard of care regimen. Understanding the underlying invasive behaviors that support tumor growth may allow for generation of novel GBM therapies. Zebrafish (Danio rerio) are attractive for genetics and live imaging, and have in recent years, emerged as a model system suitable for cancer biology research. While other groups have studied CNS tumors using zebrafish, few have concentrated on the invasive behaviors supporting the development of these diseases. Previous studies demonstrated that one of the main mechanisms of GBM invasion is perivascular invasion, i.e. single tumor cell migration along blood vessels. Here, we characterize phenotypes, methodology, and potential therapeutic avenues for utilizing zebrafish to model perivascular GBM invasion. Using patient derived xenolines or an adherent cell line, we demonstrate tumor expansion within the zebrafish brain. Within 24 hours post-intracranial injection, D54-MG-tdTomato glioma cells produce finger-like projections along the zebrafish brain vasculature. As few as 25 GBM cells were sufficient to promote single cell vessel co-option. Of note, these tumor-vessel interactions are CNS specific, and do not occur on pre-existing blood vessels when injected into the animal’s peripheral tissue. Tumor-vessel interactions increase over time and can be pharmacologically disrupted through inhibition of Wnt signaling. Therefore, zebrafish serve as a favorable model system to study perivascular glioma invasion, one of the deadly characteristics that make GBM so difficult to treat.

scholarly journals Two-color fluorescent in situ hybridization in the embryonic zebrafish brain using differential detection systems

2011 ◽  
Vol 11 (1) ◽  
pp. 43 ◽  
Author(s):  
Gilbert Lauter ◽  
Iris Söll ◽  
Giselbert Hauptmann
Keyword(s):  
In Situ Hybridization ◽  
Fluorescent In Situ Hybridization ◽  
Differential Detection ◽  
Zebrafish Brain ◽  
Detection Systems

scholarly journals Critical Effects on Akt Signaling in Adult Zebrafish Brain Following Alterations in Light Exposure

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 637
Author(s):  
Nicholas S. Moore ◽  
Robert A. Mans ◽  
Mackenzee K. McCauley ◽  
Colton S. Allgood ◽  
Keri A. Barksdale
Keyword(s):  
Optic Tectum ◽  
Visual Processing ◽  
Environmental Enrichment ◽  
Glycogen Synthase ◽  
Light Exposure ◽  
Hsp70 Expression ◽  
Light Cycle ◽  
Adult Zebrafish ◽  
Sleep State ◽  
Zebrafish Brain

Evidence from human and animal studies indicate that disrupted light cycles leads to alterations of the sleep state, poor cognition, and the risk of developing neuroinflammatory and generalized health disorders. Zebrafish exhibit a diurnal circadian rhythm and are an increasingly popular model in studies of neurophysiology and neuropathophysiology. Here, we investigate the effect of alterations in light cycle on the adult zebrafish brain: we measured the effect of altered, unpredictable light exposure in adult zebrafish telencephalon, homologous to mammalian hippocampus, and the optic tectum, a significant visual processing center with extensive telencephalon connections. The expression of heat shock protein-70 (HSP70), an important cell stress mediator, was significantly decreased in optic tectum of adult zebrafish brain following four days of altered light exposure. Further, pSer473-Akt (protein kinase B) was significantly reduced in telencephalon following light cycle alteration, and pSer9-GSK3β (glycogen synthase kinase-3β) was significantly reduced in both the telencephalon and optic tectum of light-altered fish. Animals exposed to five minutes of environmental enrichment showed significant increase in pSer473Akt, which was significantly attenuated by four days of altered light exposure. These data show for the first time that unpredictable light exposure alters HSP70 expression and dysregulates Akt-GSK3β signaling in the adult zebrafish brain.

scholarly journals The lipid-lowering drug fenofibrate combined with si-HOTAIR can effectively inhibit the proliferation of gliomas

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Wei Zhu ◽  
Hongyang Zhao ◽  
Fenfen Xu ◽  
Bin Huang ◽  
Xiaojing Dai ◽  
...  
Keyword(s):  
Noncoding Rna ◽  
Glioma Cells ◽  
Lipid Lowering ◽  
Fibric Acid Derivative ◽  
Peroxisome Proliferator ◽  
Glioma Invasion ◽  
Peroxisome Proliferator Activated Receptor ◽  
Lncrna Hotair

Abstract Background Fenofibrate is a fibric acid derivative known to have a lipid-lowering effect. Although fenofibrate-induced peroxisome proliferator-activated receptor alpha (PPARα) transcription activation has been shown to play an important role in the malignant progression of gliomas, the underlying mechanisms are poorly understood. Methods In this study, we analyzed TCGA database and found that there was a significant negative correlation between the long noncoding RNA (lncRNA) HOTAIR and PPARα. Then, we explored the molecular mechanism by which lncRNA HOTAIR regulates PPARα in cell lines in vitro and in a nude mouse glioma model in vivo and explored the effect of the combined application of HOTAIR knockdown and fenofibrate treatment on glioma invasion. Results For the first time, it was shown that after knockdown of the expression of HOTAIR in gliomas, the expression of PPARα was significantly upregulated, and the invasion and proliferation ability of gliomas were obviously inhibited. Then, glioma cells were treated with both the PPARα agonist fenofibrate and si-HOTAIR, and the results showed that the proliferation and invasion of glioma cells were significantly inhibited. Conclusions Our results suggest that HOTAIR can negatively regulate the expression of PPARα and that the combination of fenofibrate and si-HOTAIR treatment can significantly inhibit the progression of gliomas. This introduces new ideas for the treatment of gliomas.

scholarly journals Internal contact modeling for finite strain topology optimization

2021 ◽  
Author(s):  
Gore Lukas Bluhm ◽  
Ole Sigmund ◽  
Konstantinos Poulios
Keyword(s):  
Topology Optimization ◽  
Finite Strain ◽  
Contact Modeling ◽  
Internal Contact

Contact modeling in forging simulation

2002 ◽  
Vol 125-126 ◽  
pp. 583-587 ◽  
Author(s):  
B Boroomand ◽  
J Parvizian ◽  
A.R Pishevar
Keyword(s):  
Contact Modeling

P1-015: The zebrafish brain proteome project

2009 ◽  
Vol 5 (4S_Part_6) ◽  
pp. P176-P176
Author(s):  
Alexandra V. Abramsson ◽  
Ann Brinkmalm ◽  
Malin E. Andersson ◽  
Chen Gang ◽  
Gunnar Brinkmalm ◽  
...  
Keyword(s):  
Zebrafish Brain ◽  
Brain Proteome
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