Junin virus‐induced astrocytosis is impaired by iNOS inhibition

Gómez, Ricardo Martín; Yep, Alejandra; Schattner, Mirta; Berría, María I.

doi:10.1002/jmv.10254

Cited by 24 publications

(25 citation statements)

References 30 publications

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“…This is also consistent with earlier studies which demonstrated that astrocyte development occurs in late embryonic stages and is completed by the end of the first postnatal week, prior to the peak of oligodendrocyte generation (Skoff et al, 1990;Gomez et al, 2003).…”

Section: Egfpsupporting

confidence: 93%

Age-dependent fate and lineage restriction of single NG2 cells

et al. 2011

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SUMMARYNG2-expressing glia (NG2 cells, polydendrocytes) appear in the embryonic brain, expand perinatally, and persist widely throughout the gray and white matter of the mature central nervous system. We have previously reported that NG2 cells generate oligodendrocytes in both gray and white matter and a subset of protoplasmic astrocytes in the gray matter of the ventral forebrain and spinal cord. To investigate the temporal changes in NG2 cell fate, we generated NG2creER TM BAC transgenic mice, in which tamoxifen-inducible Cre is expressed in NG2 cells. Cre induction at embryonic day 16.5, postnatal day (P) 2, P30 and P60 in mice that were double transgenic for NG2creER TM BAC and the Cre reporter revealed that NG2 cells in the postnatal brain generate only NG2 cells or oligodendrocytes, whereas NG2 cells in the embryonic brain generate protoplasmic astrocytes in the gray matter of the ventral forebrain in addition to oligodendrocytes and NG2 cells. Analysis of cell clusters from single NG2 cells revealed that more than 80% of the NG2 cells in the P2 brain give rise to clusters consisting exclusively of oligodendrocytes, whereas the majority of the NG2 cells in the P60 brain generate clusters that contain only NG2 cells or a mixture of oligodendrocytes and NG2 cells. Furthermore, live cell imaging of single NG2 cells from early postnatal brain slices revealed that NG2 cells initially divide symmetrically to produce two daughter NG2 cells and that differentiation into oligodendrocytes occurred after 2-3 days.

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Section: Egfpsupporting

confidence: 93%

Age-dependent fate and lineage restriction of single NG2 cells

et al. 2011

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“…In contrast to JUNV infection of human astrocytes, a protective role of JUNV-stimulated astrogliosis dependent on the increased expression of inducible nitric oxide synthase (iNOS) and not associated with the induction of apoptosis was reported in those studies [58,63]. This discrepancy could be attributed to the different mechanisms of JUNV interaction with cells of resistant or permissive hosts.…”

Section: Discussionmentioning

confidence: 94%

Reactive astrogliosis in response to hemorrhagic fever virus: microarray profile of Junin virus-infected human astrocytes

Kolokoltsova

Yun

Paessler

2014

Virol J

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BackgroundArenavirus Junin is the causative agent of Argentine hemorrhagic fever. Limited information is available concerning the pathogenesis of this human disease, especially the pathogenesis of acute and late neurological symptoms.MethodsIn our study we present for the first time cDNA microarray profile of human astrocytes infected with the virulent strain of Junin virus. Transcriptional profiling was confirmed by quantitative real-time RT-PCR and cytokine/chemokine/growth factor assay.ResultsWe demonstrated the impact of virus infection on immune/inflammatory response/interferon signaling and apoptosis. Pro-apoptotic response and amplification with time of pro-inflammatory cascade of human astrocytes suggested neurodegenerative dysfunctional reactive astrogliosis in response to Junin virus infection.ConclusionOur results suggest potential pathogenic role of astroglial cells in the development of neurological symptoms and late neurological syndrome during Argentine hemorrhagic fever.

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“…An alternative mechanism is suggested by studies in Junin arenavirus and Sindbis alphavirus (57). In both models, inhibition of iNOS did not impact viral load but increased virus-induced pathology (38). In the arenavirus study, decreased mortality was associated with increased astrocytosis, whereas in mice infected with encephalomyelitic Sindbis alphavirus, specific inhibition of iNOS with N G -nitro-Larginine methyl ester decreased the survival of infected neurons (57).…”

Section: Discussionmentioning

confidence: 99%

CpG Oligodeoxynucleotides Protect Newborn Mice from a Lethal Challenge with the Neurotropic Tacaribe Arenavirus

Pedras-Vasconcelos

Goucher

Puig

et al. 2006

The Journal of Immunology

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The innate immune system is key to limiting the early spread of most pathogens and directing the development of Ag-specific immunity. Recently, a number of synthetic molecules that activate the innate immune system by stimulating TLRs have been identified. Among them, synthetic oligodeoxynucleotides (ODNs) containing unmethylated CpG motifs (CpG ODNs) were shown to activate TLR9-bearing B cells, macrophages, and dendritic cells to induce a strong proinflammatory milieu and a type 1-biased immune response that protects mice from a variety of parasitic, bacterial, and viral infections. Although the protective effect of CpG ODN in adult mice was well established, its effectiveness in neonates, which have lower numbers of dendritic, B, and T cells and tend to favor Th2 responses, was unclear. This study uses the New World arenavirus Tacaribe, a neurotropic pathogen that is lethal in newborn mice, to explore the effectiveness of TLR-mediated innate immune responses. Neonatal BALB/c mice treated with CpG ODN at the time of infection had reduced viral load (p < 0.01) and increased survival (52%, p < 0.001 i.p.; 36%, p < 0.05 intranasally). Protection was achieved in mice treated no later than 3 days postchallenge and appears to be mediated by an increase in Ag-specific Abs (IgG and IgM) and to require inducible NO synthase expression and NO production. To our knowledge, this is the first study assessing the mechanisms by which CpG ODN can protect mice from a neurotropic viral infection.

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Junin virus‐induced astrocytosis is impaired by iNOS inhibition

Cited by 24 publications

References 30 publications

Age-dependent fate and lineage restriction of single NG2 cells

Age-dependent fate and lineage restriction of single NG2 cells

Reactive astrogliosis in response to hemorrhagic fever virus: microarray profile of Junin virus-infected human astrocytes

CpG Oligodeoxynucleotides Protect Newborn Mice from a Lethal Challenge with the Neurotropic Tacaribe Arenavirus

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