scholarly journals Resistance to DNA Damaging Agents Produced Invasive Phenotype of Rat Glioma Cells—Characterization of a New in Vivo Model

Molecules ◽  
2016 ◽  
Vol 21 (7) ◽  
pp. 843 ◽  
Author(s):  
Sonja Stojković ◽  
Ana Podolski-Renić ◽  
Jelena Dinić ◽  
Željko Pavković ◽  
Jose Ayuso ◽  
...  
Keyword(s):  
Glioma Cells ◽  
In Vivo Model ◽  
Invasive Phenotype ◽  
Rat Glioma ◽  
Dna Damaging Agents

scholarly journals Cytosolic Activation of Cathepsins Mediates Parvovirus H-1-Induced Killing of Cisplatin and TRAIL-Resistant Glioma Cells

2007 ◽  
Vol 81 (8) ◽  
pp. 4186-4198 ◽  
Author(s):  
Matteo Di Piazza ◽  
Carmen Mader ◽  
Karsten Geletneky ◽  
Marta Herrero y Calle ◽  
Ekkehard Weber ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Glioma Cells ◽  
Rat Glioma ◽  
Dna Damaging Agents ◽  
Passage Number ◽  
Infected Cells ◽  
Normal Human ◽  
Low Passage

ABSTRACT Gliomas are often resistant to the induction of apoptotic cell death as a result of the development of survival mechanisms during astrocyte malignant transformation. In particular, the overexpression of Bcl-2-family members interferes with apoptosis initiation by DNA-damaging agents (e.g., cisplatin) or soluble death ligands (e.g., TRAIL). Using low-passage-number cultures of glioma cells, we have shown that parvovirus H-1 is able to induce death in cells resistant to TRAIL, cisplatin, or both, even when Bcl-2 is overexpressed. Parvovirus H-1 triggers cell death through both the accumulation of lysosomal cathepsins B and L in the cytosol of infected cells and the reduction of the levels of cystatin B and C, two cathepsin inhibitors. The impairment of either of these effects protects glioma cells from the viral lytic effect. In normal human astrocytes, parvovirus H-1 fails to induce a killing mechanism. In vivo, parvovirus H-1 infection of rat glioma cells intracranially implanted into recipient animals triggers cathepsin B activation as well. This report identifies for the first time cellular effectors of the killing activity of parvovirus H-1 against malignant brain cells and opens up a therapeutic approach which circumvents their frequent resistance to other death inducers.

scholarly journals Chloroquine enhances temozolomide cytotoxicity in malignant gliomas by blocking autophagy

2014 ◽  
Vol 37 (6) ◽  
pp. E12 ◽  
Author(s):  
Encouse B. Golden ◽  
Hee-Yeon Cho ◽  
Ardeshir Jahanian ◽  
Florence M. Hofman ◽  
Stan G. Louie ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Malignant Gliomas ◽  
Glioma Cells ◽  
In Vivo Model ◽  
Autophagosome Formation ◽  
Individual Drug ◽  
In Vivo Experiments ◽  
Associated Proteins

Object In a recent clinical trial, patients with newly diagnosed glioblastoma multiforme benefited from chloroquine (CQ) in combination with conventional therapy (resection, temozolomide [TMZ], and radiation therapy). In the present study, the authors report the mechanism by which CQ enhances the therapeutic efficacy of TMZ to aid future studies aimed at improving this therapeutic regimen. Methods Using in vitro and in vivo experiments, the authors determined the mechanism by which CQ enhances TMZ cytotoxicity. They focused on the inhibition-of-autophagy mechanism of CQ by knockdown of the autophagy-associated proteins or treatment with autophagy inhibitors. This mechanism was tested using an in vivo model with subcutaneously implanted U87MG tumors from mice treated with CQ in combination with TMZ. Results Knockdown of the autophagy-associated proteins (GRP78 and Beclin) or treatment with the autophagy inhibitor, 3-methyl adenine (3-MA), blocked autophagosome formation and reduced CQ cytotoxicity, suggesting that autophagosome accumulation precedes CQ-induced cell death. In contrast, blocking autophagosome formation with knockdown of GRP78 or treatment with 3-MA enhanced TMZ cytotoxicity, suggesting that the autophagy pathway protects from TMZ-induced cytotoxicity. CQ in combination with TMZ significantly increased the amounts of LC3B-II (a marker for autophagosome levels), CHOP/GADD-153, and cleaved PARP (a marker for apoptosis) over those with untreated or individual drug-treated glioma cells. These molecular mechanisms seemed to take place in vivo as well. Subcutaneously implanted U87MG tumors from mice treated with CQ in combination with TMZ displayed higher levels of CHOP/GADD-153 than did untreated or individual drug-treated tumors. Conclusions Taken together, these results demonstrate that CQ blocks autophagy and triggers endoplasmic reticulum stress, thereby increasing the chemosensitivity of glioma cells to TMZ.

scholarly journals Characterization of the Structural and Functional Determinants of MANF/CDNF in Drosophila In Vivo Model

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e73928 ◽  
Author(s):  
Riitta Lindström ◽  
Päivi Lindholm ◽  
Jukka Kallijärvi ◽  
Li-ying Yu ◽  
T. Petteri Piepponen ◽  
...  
Keyword(s):  
In Vivo Model

P0975 : Characterization of an in vivo model of juvenile non-alcoholic fatty liver disease

2015 ◽  
Vol 62 ◽  
pp. S711-S712
Author(s):  
V. Marin ◽  
N. Rosso ◽  
M. Dal Ben ◽  
A. Raseni ◽  
C. Degrassi ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
In Vivo Model ◽  
Alcoholic Fatty Liver ◽  
Alcoholic Fatty Liver Disease

scholarly journals ENHANCED FLUORESCENCE IMAGING WITH DMSO-MEDIATED OPTICAL CLEARING

2010 ◽  
Vol 03 (03) ◽  
pp. 153-158 ◽  
Author(s):  
SANJEEV KARMA ◽  
JAMES HOMAN ◽  
CHARLES STOIANOVICI ◽  
BERNARD CHOI
Keyword(s):  
Fluorescence Emission ◽  
Model Systems ◽  
In Vivo Studies ◽  
In Vivo Model ◽  
Fluorescence Signal ◽  
Optical Clearing ◽  
Treated Site

Recent studies have demonstrated that topical application of glycerol on intact skin does not affect its optical scattering properties. Investigators from our research group recently revisited the use of dimethyl sulfoxide (DMSO) as an agent with optical clearing potential. We address the use of optical clearing to enhance quantitation of subsurface fluorescence emission. We employed both in vitro and in vivo model systems to study the effect of topical DMSO application on fluorescence emission. Our in vitro experiments performed on a tissue-simulating phantom suggest that DMSO-mediated optical clearing enables enhanced characterization of subsurface fluorophores. With topical DMSO application, a marked increase in fluorescence emission was observed. After 30 min, the fluorescence signal at the DMSO-treated site was 9× greater than the contralateral saline-treated site. This ratio increased to 13× at 105 min after agent application. In summary, DMSO is an effective optical clearing agent for improved fluorescence emission quantitation and warrants further study in preclinical in vivo studies. Based on outcomes from previous clinical studies on the toxicity profile of DMSO, we postulate that clinical application of DMSO as an optical clearing agent, can be performed safely, although further study is warranted.

scholarly journals Restoration of p53 function for selective Fas-mediated apoptosis in human and rat glioma cells in vitro and in vivo by a p53 COOH-terminal peptide

2006 ◽  
Vol 5 (1) ◽  
pp. 20-28 ◽  
Author(s):  
Patrick B. Senatus ◽  
Yin Li ◽  
Christopher Mandigo ◽  
Gwen Nichols ◽  
Gaetan Moise ◽  
...  
Keyword(s):  
Glioma Cells ◽  
Rat Glioma

181. Development and Characterization of a Novel In Vivo Model for Carcinoid Syndrome

2009 ◽  
Vol 151 (2) ◽  
pp. 255
Author(s):  
L.N. Jackson ◽  
L.A. Chen ◽  
S.D. Larson ◽  
S.R. Silva ◽  
P.G. Rychahou ◽  
...  
Keyword(s):  
Carcinoid Syndrome ◽  
In Vivo Model
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