Theiler's murine encephalomyelitis virus infection of astrocytes induces the expression of chemokines which attract activated but not resting T lymphocytes.

In this article, we studied the production of the chemokine CXCL9, also termed Mig (monokine induced by gamma interferon) by cultured SJL/J mouse astrocytes infected with the BeAn strain of Theiler's murine encephalomyelitis virus (TMEV). This picornavirus induces demyelination in the SJL/J genetically susceptible strain of mice through an immune process mediated by CD4 Th1 T cells. Those cells were chemoattracted by chemokines inside the central nervous system (CNS) after blood-brain barrier (BBB) disruption.

Kir 4.1 inward rectifier potassium channel is upregulated in astrocytes in a murine multiple sclerosis model.

Multiple sclerosis (MS) is a high prevalence degenerative disease characterized at the cellular level by glial and neuronal cell death. The causes of cell death during the disease course are not fully understood. In this work we demonstrate that in a MS model induced by Theiler's murine encephalomyelitis virus (TMEV) infection, the inward rectifier (Kir) 4.

Overexpression of caspase 1 in apoptosis-resistant astrocytes infected with the BeAn Theiler's virus.

In this study, we demonstrate the upregulation in the expression of caspases 1 and 11 by SJL/J mouse brain astrocytes infected with the BeAn strain of Theiler's murine encephalomyelitis virus (TMEV). The upregulation of both proteases hints at protection of astrocytic cells from apoptotic death. We therefore looked for the reason of the demonstrated absence of programmed cell death in BeAn-infected SJL/J astrocytes.

Theiler's virus infection provokes the overexpression of genes coding for the chemokine Ip10 (CXCL10) in SJL/J murine astrocytes, which can be inhibited by modulators of estrogen receptors.

Theiler's murine encephalomyelitis virus (TMEV) induces demyelination in susceptible strains of mice (SJL/J) through an immunopathological process that is mediated by CD4(+) Th1 T cell. These T cells are chemoattracted to the central nervous system by chemokines. Hence, in this study, we focused on the production of the chemokine "interferon-gamma-inducible protein 10 kDa," or IP-10/CXCL10, by cultured SJL/J mouse astrocytes infected with the BeAn strain of TMEV and its capacity to attract activated T cells.

Survivin prevents apoptosis by binding to caspase-3 in astrocytes infected with the BeAn strain of Theiler's murine encephalomyelitis virus.

This paper reports the upregulation of the gene coding for the apoptosis regulator family member "surviving" in SJL/J mouse brain astrocyte cultures infected with the BeAn strain of TMEV. cRNA from mock- and TMEV-infected SJL/J astrocytes was hybridised to an Affymetrix whole murine genome DNA microarray. Analysis revealed the upregulation of two sequences coding for the survivin protein in infected cells; this was confirmed by RT-PCR and qPCR.

An in vitro experimental model of neuroinflammation: the induction of interleukin-6 in murine astrocytes infected with Theiler's murine encephalomyelitis virus, and its inhibition by oestrogenic receptor modulators.

This paper describes an experimental model of neuroinflammation based on the production of interleukin-6 (IL-6) by neural glial cells infected with Theiler's murine encephalomyelitis virus (TMEV). Production of IL-6 mRNA in mock-infected and TMEV-infected SJL/J murine astrocytes was examined using the Affymetrix murine genome U74v2 DNA microarray. The IL-6 mRNA from infected cells showed an eightfold increase in hybridization to a sequence encoding IL-6 located on chromosome number 5.

Up-regulation of the vascular cell adhesion molecule-1 (VCAM-1) induced by Theiler's murine encephalomyelitis virus infection of murine brain astrocytes.

The present article reports the up-regulation of the expression of the vascular cell adhesion molecule-1 (VCAM-1) by SJL/J mouse brain astrocytes infected with Theiler's murine encephalomyelitis virus (TMEV). Complementary RNA (cRNA) from mock- and TMEV-infected cells was hybridized to the Affymetrix whole murine genome U74v2 DNA microarray. Hybridization data analysis revealed background expression in untreated cells and the up-regulation of three sequences coding for VCAM-1, as described by the SCOP (Structural Classification Of Proteins) database.

Interferon-alpha/beta genes are up-regulated in murine brain astrocytes after infection with Theiler's murine encephalomyelitis virus.

This article reports the production of interferon alpha/beta (IFN-alpha/beta) by SJL/J mouse brain astrocyte cultures infected with Theiler's murine encephalomyelitis virus (TMEV). cRNA from mock- and TMEV-infected SJL/J astrocytes was hybridized to the Affymetrix whole murine genome DNA microarray. Analysis revealed the up-regulation of 3 sequences coding for the IFN-alpha/beta domain.

Over-expression of GTP-binding proteins and GTPase activity in mouse astrocyte membranes in response to Theiler's murine encephalomyelitis virus infection.

Intracerebral infection with Theiler's murine encephalomyelitis virus (TMEV) induces a demyelinating disease that resembles human multiple sclerosis. In order to delineate the early events in this virus-induced neuroinflammatory disease, we have analyzed global GTPases gene activation following TMEV infection of murine brain astrocytes. DNA hybridization microchip analysis demonstrated that 10 sequences described as GTPbinding proteins and GTPases in different protein databases were over-expressed, in response to this infectious agent in astroglial cells.

Induction of the CXCL1 (KC) chemokine in mouse astrocytes by infection with the murine encephalomyelitis virus of Theiler.

In the present study, we focused on the production of the chemokine CXCL1, also termed KC, by cultured Theiler murine encephalomyelitis virus (TMEV)-infected mouse astrocytes. cRNA from mock- and TMEV-infected cells was hybridized to the Affymetrix murine genome U74v2 DNA microarray. Hybridization data analysis demonstrated upregulation of two sequences coding for IL-8 and related to the GRO 1 oncogene MGSA.

Theiler's virus induces the MIP-2 chemokine (CXCL2) in astrocytes from genetically susceptible but not from resistant mouse strains.

The murine encephalomyelitis virus of Theiler (TMEV) induces demyelination in susceptible strains of mice by a CD4(+) Th1 T cell mediated immunopathologic process. We focused on the production of one chemokine, the macrophage inflammatory protein-2 (MIP-2 or CXCL2), by cultured mouse astrocytes infected with the BeAn strain of TMEV. Analysis of a murine genome DNA hybridized with cRNA from mock- and TMEV-infected astrocytes, revealed up-regulation of three sequences encoding MIP-2.

In vitro myelination by oligodendrocyte precursor cells transfected with the neurotrophin-3 gene.

Oligodendrocyte precursor cells require exogenous neurotrophin-3 (NT-3) for differentiation into oligodendrocytes. We transfected precursor cells with the gene for NT-3 and looked for changes in their development into myelin-forming cells. The expression of NT-3 in transfected cells was demonstrated by reverse transcription followed by PCR as well as by Northern blots.

High-neurovirulence GDVII virus induces apoptosis in murine astrocytes through tumor necrosis factor (TNF)-receptor and TNF-related apoptosis-inducing ligand.

We carried out a study to determine if the high-neurovirulence GDVII strain of Theiler's murine encephalomyelitis virus (TMEV) and the demyelinating, low-neurovirulence BeAn strain induced apoptosis in murine astrocytes. Astrocytes, the major glial cell population of the central nervous system, were semipermissive for GDVII virus replication. Programmed cell death, demonstrated by apoptosis-specific caspase-3 protease activity, was maximal 8 h after GDVII infection at an m.

Binding of adenovirus to its receptors in mouse astrocytes induces c-fos proto-oncogene and apoptosis.

We have demonstrated that Ad.betaGal, a broadly used adenoviral vector of serotype 5, binds and induces proto-oncogene c-fos expression in quiescent cultures of mouse brain astrocytes. As observed in Northern blots, the expression of this immediate early gene is induced by viral infection in a dose-dependent manner, peaking at a multiplicity of infection (m.