scholarly journals Cystathionine Promotes the Proliferation of Human Astrocytoma U373 Cells

2018 ◽  
Vol 38 (6) ◽  
pp. 3501-3505 ◽  
Author(s):  
HALINA JURKOWSKA ◽  
MARIA WRÓBEL
Keyword(s):  
Human Astrocytoma ◽  
U373 Cells

scholarly journals Requirements for Measles Virus Induction of RANTES Chemokine in Human Astrocytoma-Derived U373 Cells

1999 ◽  
Vol 73 (4) ◽  
pp. 3117-3124 ◽  
Author(s):  
Katherine H. Noe ◽  
Cristina Cenciarelli ◽  
Sue A. Moyer ◽  
Paul A. Rota ◽  
Moon L. Shin
Keyword(s):  
Membrane Fusion ◽  
Measles Virus ◽  
Critical Role ◽  
A549 Cells ◽  
Dependent Manner ◽  
Virus Binding ◽  
Viral Protein Synthesis ◽  
Nucleocapsid Gene ◽  
Human Astrocytoma ◽  
U373 Cells

ABSTRACT Interferons and chemokines play a critical role in regulating the host response to viral infection. Measles virus, a member of theParamyxoviridae family, induces RANTES expression by astrocytes. We have examined the mechanism of this induction in U373 cells derived from a human astrocytoma. RANTES was induced in a dose- and time-dependent manner by measles virus infection. Inhibition of receptor binding by the anti-CD46 antibody TRA-2.10 and of virus-membrane fusion by the tripeptide X-Phe-Phe-Gly reduced RANTES expression. Formalin-inactivated virus, which can bind but not fuse, and extensively UV-irradiated virus, which can bind and fuse, were both ineffective. Therefore, virus binding to the cellular receptor CD46 and subsequent membrane fusion were necessary, but not sufficient, to induce RANTES. UV irradiation of virus for less than 10 min proportionally inhibited viral transcription and RANTES expression. RANTES induction was decreased in infected cells treated with ribavirin, which inhibits measles virus transcription. However, RANTES mRNA was superinduced by measles virus in the presence of cycloheximide. These data suggest that partial transcription of the viral genome is sufficient and necessary for RANTES induction, whereas viral protein synthesis and replication are not required. This hypothesis was supported by the fact that RANTES was induced through transient expression of the measles virus nucleocapsid gene but not by measles genes encoding P or L proteins or by leader RNA in A549 cells. Thus, transcription of specific portions of measles virus RNA, such as the nucleocapsid gene, appears able to generate the specific signaling required to induce RANTES gene expression.

scholarly journals Progesterone Induces the Growth and Infiltration of Human Astrocytoma Cells Implanted in the Cerebral Cortex of the Rat

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Liliana Germán-Castelán ◽  
Joaquín Manjarrez-Marmolejo ◽  
Aliesha González-Arenas ◽  
María Genoveva González-Morán ◽  
Ignacio Camacho-Arroyo
Keyword(s):  
Motor Cortex ◽  
Male Rats ◽  
Astrocytoma Cells ◽  
Intracellular Receptor ◽  
Human Astrocytoma ◽  
And Migration ◽  
Astrocytoma Grade Iii ◽  
Antagonist Ru486 ◽  
U373 Cells ◽  
Human Astrocytoma Cells

Progesterone (P4) promotes cell proliferation in several types of cancer, including brain tumors such as astrocytomas, the most common and aggressive primary intracerebral neoplasm in humans. In this work, we studied the effects of P4and its intracellular receptor antagonist, RU486, on growth and infiltration of U373 cells derived from a human astrocytoma grade III, implanted in the motor cortex of adult male rats, using two treatment schemes. In the first one, fifteen days after cells implantation, rats were daily subcutaneously treated with vehicle (propylene glycol, 160 μL), P4(1 mg), RU486 (5 mg), or P4+ RU486 (1 mg and 5 mg, resp.) for 21 days. In the second one, treatments started 8 weeks after cells implantation and lasted for 14 days. In both schemes we found that P4significantly increased the tumor area as compared with the rest of the treatments, whereas RU486 blocked P4effects. All rats treated with P4showed tumor infiltration, while 28.6% and 42.9% of the animals treated with RU486 and P4+ RU486, respectively, presented it. Our data suggest that P4promotes growth and migration of human astrocytoma cells implanted in the motor cortex of the rat through the interaction with its intracellular receptor.

scholarly journals Nitric Oxide Modulation of Interleukin-1β-Evoked Intracellular Ca2+Release in Human Astrocytoma U-373 MG Cells and Brain Striatal Slices

2000 ◽  
Vol 20 (24) ◽  
pp. 8980-8986 ◽  
Author(s):  
Antonella Meini ◽  
Alberto Benocci ◽  
Maria Frosini ◽  
Gianpietro Sgaragli ◽  
Gianpaolo Pessina ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Interleukin 1Β ◽  
Striatal Slices ◽  
Human Astrocytoma

scholarly journals Discrimination of Human Astrocytoma Subtypes by Lipid Analysis Using Desorption Electrospray Ionization Imaging Mass Spectrometry

2010 ◽  
Vol 122 (34) ◽  
pp. 6089-6092 ◽  
Author(s):  
Livia S. Eberlin ◽  
Allison L. Dill ◽  
Alexandra J. Golby ◽  
Keith L. Ligon ◽  
Justin M. Wiseman ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Electrospray Ionization ◽  
Lipid Analysis ◽  
Imaging Mass Spectrometry ◽  
Desorption Electrospray Ionization ◽  
Human Astrocytoma

Cdk5 mediates changes in morphology and promotes apoptosis of astrocytoma cells in response to heat shock

2001 ◽  
Vol 114 (6) ◽  
pp. 1145-1153 ◽  
Author(s):  
C. Gao ◽  
S. Negash ◽  
H.S. Wang ◽  
D. Ledee ◽  
H. Guo ◽  
...  
Keyword(s):  
Heat Shock ◽  
Cell Line ◽  
Fluorescent Protein ◽  
Morphological Changes ◽  
Normal Growth ◽  
Dominant Negative ◽  
Specific Expression ◽  
Cell Matrix ◽  
Dominant Negative Mutation ◽  
U373 Cells

The cyclin-dependent kinase member, Cdk5, is expressed in a variety of cell types, but neuron-specific expression of its activator, p35, is thought to limit its activity to neurons. Here we demonstrate that both Cdk5 and p35 are expressed in the human astrocytoma cell line, U373. Cdk5 and p35 are present in the detergent-insoluble cytoskeletal fraction of this cell line and Cdk5 localizes to filopodia and vinculin-rich regions of cell-matrix contact in lamellopodia. When exposed to a 46(o)C heat shock, U373 cells change shape, lose cell-matrix contacts and show increased levels of apoptosis. To test whether Cdk5 activation might play a role in these events, U373 cells were stably transfected with histidine-tagged or green fluorescent protein-tagged constructs of Cdk5 or a dominant negative mutation, Cdk5T33. Under normal growth conditions, growth characteristics of the stably transfected lines were indistinguishable from untransfected U373 cells and Cdk5 localization was not changed. However, when subjected to heat shock, cells stably transfected with Cdk5-T33 remained flattened, showed little loss of cell-matrix adhesion, and exhibited significantly lower levels of apoptosis. In contrast, cells that overexpressed wild-type Cdk5 showed morphological changes similar to those seen in untransfected U373 cells in response to heat shock and had significantly higher levels of apoptosis. Heat-shocked cells showed changes in p35 mobility and stability of the Cdk5/p35 complex consistent with endogenous Cdk5 activity. Together these findings suggest that endogenous Cdk5 activity may play a key role in regulating morphology, attachment, and apoptosis in U373 cells, and raise the possibility that Cdk5 may be a general regulator of cytoskeletal organization and cell adhesion in both neuronal and non-neuronal cells.

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