Immunohistochemical detection of metalloproteinase-9 (MMP-9), anti-oxidant like 1 protein (AOP-1) and synaptosomal-associated protein (SNAP-25) in the cerebella of dogs naturally infected with spontaneous canine distemper

Bregano, Lívia C.; Agostinho, Sabrina D.; Roncatti, Flávio L.B.T.; Pires, Marcília C.; Riva, Henrique Guimarães; Luvizotto, Maria Cecília Rui; Cardoso, Tereza Cristina

doi:10.5603/fhc.2011.0007

Cited by 5 publications

(4 citation statements)

References 22 publications

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“…Spontaneous CDV infection leads to changes in the expression of certain MMPs and TIMPs, depending on the stage of the disease [61,71,72]. Most notably, and similar to observations on cytokine expression, a prominent up-regulation of several MMPs and TIMPs is observed in acute and subacute lesions prior to inflammatory changes.…”

Section: Canine Distemper Leukoencephalitis — Novel Aspects Of Itsmentioning

confidence: 80%

New Aspects of the Pathogenesis of Canine Distemper Leukoencephalitis

Lempp

Spitzbarth

Puff

et al. 2014

Viruses

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Canine distemper virus (CDV) is a member of the genus morbillivirus, which is known to cause a variety of disorders in dogs including demyelinating leukoencephalitis (CDV-DL). In recent years, substantial progress in understanding the pathogenetic mechanisms of CDV-DL has been made. In vivo and in vitro investigations provided new insights into its pathogenesis with special emphasis on axon-myelin-glia interaction, potential endogenous mechanisms of regeneration, and astroglial plasticity. CDV-DL is characterized by lesions with a variable degree of demyelination and mononuclear inflammation accompanied by a dysregulated orchestration of cytokines as well as matrix metalloproteinases and their inhibitors. Despite decades of research, several new aspects of the neuropathogenesis of CDV-DL have been described only recently. Early axonal damage seems to represent an initial and progressive lesion in CDV-DL, which interestingly precedes demyelination. Axonopathy may, thus, function as a potential trigger for subsequent disturbed axon-myelin-glia interactions. In particular, the detection of early axonal damage suggests that demyelination is at least in part a secondary event in CDV-DL, thus challenging the dogma of CDV as a purely primary demyelinating disease. Another unexpected finding refers to the appearance of p75 neurotrophin (NTR)-positive bipolar cells during CDV-DL. As p75NTR is a prototype marker for immature Schwann cells, this finding suggests that Schwann cell remyelination might represent a so far underestimated endogenous mechanism of regeneration, though this hypothesis still remains to be proven. Although it is well known that astrocytes represent the major target of CDV infection in CDV-DL, the detection of infected vimentin-positive astrocytes in chronic lesions indicates a crucial role of this cell population in nervous distemper. While glial fibrillary acidic protein represents the characteristic intermediate filament of mature astrocytes, expression of vimentin is generally restricted to immature or reactive astrocytes. Thus, vimentin-positive astrocytes might constitute an important cell population for CDV persistence and spread, as well as lesion progression. In vitro models, such as dissociated glial cell cultures, as well as organotypic brain slice cultures have contributed to a better insight into mechanisms of infection and certain morphological and molecular aspects of CDV-DL. Summarized, recent in vivo and in vitro studies revealed remarkable new aspects of nervous distemper. These new perceptions substantially improved our understanding of the pathogenesis of CDV-DL and might represent new starting points to develop novel treatment strategies.

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Section: Canine Distemper Leukoencephalitis — Novel Aspects Of Itsmentioning

confidence: 80%

New Aspects of the Pathogenesis of Canine Distemper Leukoencephalitis

Lempp

Spitzbarth

Puff

et al. 2014

Viruses

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“…However, the significant induction of ROS or the depletion of cellular antioxidants induces cell death, and ROS are likely to act as signaling intermediates that are involved in the signal transduction mechanism of apoptosis [3,22,23]. The ( AOP-1 ) functions as a thioredoxin-dependent peroxidase that scavenges ROS, such as H 2 O 2 [30,31]. Remarkably, we were only able to detect the antigens and mRNA of AOP-1 among embryos exposed to BoHV-5.…”

Section: Discussionmentioning

confidence: 99%

“…Remarkably, we were only able to detect the antigens and mRNA of AOP-1 among embryos exposed to BoHV-5. The role of AOP-1 in viral infections has previously been demonstrated; however, this is the first report of the association between AOP-1 and in vitro-produced bovine embryos [30-32]. …”

Section: Discussionmentioning

confidence: 99%

Evaluation of developmental changes in bovine in vitro produced embryos following exposure to bovine Herpesvirus type 5

Brenner

Silva-Frade

Ferrarezi

et al. 2012

Reprod Biol Endocrinol

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BackgroundBovine Herpesvirus type-5 (BoHV-5) is a neurovirulent α-Herpesvirus which is potentially pathogenic for cows and suspected to be associated with reproductive disorders. Interestingly, natural transmission of BoHV-5 by contaminated semen was recently described in Australia. Additionally, BoHV-5 was also isolated from the semen of a healthy bull in the same country and incriminated in a natural outbreak of reproductive disease after artificial insemination. In contrast with BoHV-1, experimental exposure of in vitro produced bovine embryos to BoHV-5 does not affect embryo viability and seems to inhibit some pathways of apoptosis. However, the mechanisms responsible for these phenomena are poorly understood. In this study, we examined mitochondrial activity, antioxidant protection, stress response and developmental rates of in vitro produced bovine embryos that were exposed and unexposed to BoHV-5.MethodsFor this purpose, bovine embryos produced in vitro were assayed for cell markers after experimental infection of oocytes (n = 30; five repetitions), in vitro fertilization and development. The indirect immunofluorescence was employed to measure the expression of superoxide dismutase 1 (SOD1), anti-oxidant like protein 1 (AOP-1), heat shock protein 70.1 (Hsp 70.1) and also viral antigens in embryos derived from BoHV-5 exposed and unexposed oocytes. The determination of gene transcripts of mitochondrial activity (SOD1), antioxidant protection (AOP-1) and stress response (Hsp70.1) were evaluated using the reverse transcriptase polymerase chain reaction (RT-PCR). MitoTracker Green FM, JC-1 and Hoechst 33342-staining were used to evaluate mitochondrial distribution, segregation patterns and embryos morphology. The intensity of labeling was graded semi-quantitatively and embryos considered intensively marked were used for statistical analysis.ResultsThe quality of the produced embryos was not affected by exposure to BoHV-5. Of the 357 collected oocytes, 313 (+/− 6.5; 87,7%) were cleaved and 195 (+/− 3.2; 54,6%) blastocysts were produced without virus exposure. After exposure, 388 oocytes were cleaved into 328 (+/− 8.9, 84,5%), and these embryos produced 193 (+/− 3.2, 49,7%) blastocysts. Viral DNA corresponding to the US9 gene was only detected in embryos at day 7 after in vitro culture, and confirmed by indirect immunofluorescence assay (IFA). These results revealed significant differences (p < 0.05) between exposed and unexposed oocytes fertilized, as MitoTracker Green FM staining Fluorescence intensity of Jc-1 staining was significantly higher (p < 0.005) among exposed embryos (143 +/− 8.2). There was no significant difference between the ratios of Hoechst 33342-stained nuclei and total cells in good-quality blastocysts (in both the exposed and unexposed groups). Using IFA and reverse transcriptase polymerase chain reaction (RT-PCR) for the set of target transcripts (SOD1, AOP-1 and Hsp 70.1), there were differences in the mRNA and respective proteins between the control and exposed embryos. Only the exposed em...

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“…Measurement of SNAP-25 (a presynaptic brain marker) immunoreactivity varied along the septo temporal axis of hippocampus with significant overall increases in septodorsal and mid septotemporal regions and overall decreases in temporal ventral areas of the hippocampus of E9 infected offspring (Fatemi et al, 1998). SNAP-25 has roles in axonal growth and neurotransmitter release (Grabs et al, 1996; Osen-Sand et al, 1993; Oyler et al, 1989), and also been associated with death of virally infected cells (Bregano et al, 2011). At E16, protein expression of Mbp 14 kDa isoform was significantly downregulated at P14 and Mbp 18.5 and 17.2 kDa isoforms were significantly downregulated at P56 in the cerebella of exposed offspring (Fatemi et al, 2009a).…”

Section: Animal Models Of Viral Infectionmentioning

confidence: 99%

Viral infection, inflammation and schizophrenia

Kneeland

Fatemi

2013

Progress in Neuro-Psychopharmacology and Biological Psychiatry

129

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Schizophrenia is a severe neurodevelopmental disorder with genetic and environmental etiologies. Prenatal viral/bacterial infections and inflammation play major roles in the genesis of schizophrenia. In this review, we describe a viral model of schizophrenia tested in mice whereby the offspring of mice prenatally infected with influenza at E7, E9, E16, and E18 show significant gene, protein, and brain structural abnormalities postnatally. Similarly, we describe data on rodents exposed to bacterial infection or injected with a synthetic viral mimic (PolyI:C) also demonstrating brain structural and behavioral abnormalities. Moreover, human serologic data has been indispensible in supporting the viral theory of schizophrenia. Individuals born seropositive for bacterial and viral agents are at a significantly elevated risk of developing schizophrenia. While the specific mechanisms of prenatal viral/bacterial infections and brain disorder are unclear, recent findings suggest that the maternal inflammatory response may be associated with fetal brain injury. Preventive and therapeutic treatment options are also proposed. This review presents data related to epidemiology, human serology, and experimental animal models which support the viral model of schizophrenia.

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Immunohistochemical detection of metalloproteinase-9 (MMP-9), anti-oxidant like 1 protein (AOP-1) and synaptosomal-associated protein (SNAP-25) in the cerebella of dogs naturally infected with spontaneous canine distemper

Cited by 5 publications

References 22 publications

New Aspects of the Pathogenesis of Canine Distemper Leukoencephalitis

New Aspects of the Pathogenesis of Canine Distemper Leukoencephalitis

Evaluation of developmental changes in bovine in vitro produced embryos following exposure to bovine Herpesvirus type 5

Viral infection, inflammation and schizophrenia

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