First description of enhanced expression of transforming growth factor-alpha (TGF-?) and glia maturation factor-beta (GMF-ß) correlate with severity of neuropathology in border disease virus-infected small ruminants

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dc.contributor.authorDinçel, Güngör Çağdaş
dc.contributor.authorKul, Oğuz
dc.date.accessioned13.07.201910:50:10
dc.date.accessioned2019-07-16T08:25:21Z
dc.date.available13.07.201910:50:10
dc.date.available2019-07-16T08:25:21Z
dc.date.issued2019
dc.departmentEskil Meslek Yüksekokulu
dc.descriptionPubMed ID: 30654008
dc.description.abstractBorder disease (BD) is caused by Pestivirus and characterized by severe neuropathology, and histopathologically observed severe hypomyelination. We have previously shown that small ruminants infected with border disease virus (BDV) play an important role for neuropathology and pathogenesis of severe oxidative damage in brain tissue, neuronal mtDNA; in the production of high pathologic levels of nitric oxide; in glial cell activation and stimulation of intrinsic apoptosis pathway. This study aimed to investigate the relationship between glia maturation factor beta (GMF-ß) and transforming growth factor alpha (TGF-?) expressions and the causes of BDV-induced neuropathology and to investigate their role in neuropathogenesis in a way that was not presented before. Expression levels of GMF-ß and TGF-? were investigated. Results of the study revealed that the levels of GMF-ß (P < 0.005) and TGF-? (P < 0.005) expression in the brain tissue markedly increased in the BDV-infected animals compared to the non-infected healthy control group. While TGF-? expressions were predominantly observed in neurons, GMF-ß expressions were found in astrocytes, glial cells and neurons. These results were reasonable to suggest that BDV-mediated increased GMF-ß might play a pivotal role neuropathogenesis and a different type of role in the mechanism of neurodegeneration/neuropathology in the process of BD. The results also indicated that increased levels of GMF up-regulation in glial cells and neurons causes neuronal destruction, suggesting pathological pathway involving GMF-mediated brain cell cytotoxicity. It is clearly indicated that the cause of astrogliosis is due to severe TGF-a expression. This is the first study to demonstrate the expression of GMF-ß and TGF-? in neurons and reactive glial cells and its association with neuropathology in BD. © 2019 Elsevier Ltd
dc.identifier.doi10.1016/j.micpath.2019.01.015
dc.identifier.endpage310en_US
dc.identifier.issn0882-4010
dc.identifier.scopusqualityQ1
dc.identifier.startpage301en_US
dc.identifier.urihttps://dx.doi.org/10.1016/j.micpath.2019.01.015
dc.identifier.urihttps://hdl.handle.net/20.500.12451/3037
dc.identifier.volume128en_US
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherAcademic Press
dc.relation.ispartofMicrobial Pathogenesis
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectBorder Disease
dc.subjectGMF
dc.subjectImmunopathogenesis
dc.subjectNeuropathology
dc.subjectPestivirus
dc.subjectTGF
dc.titleFirst description of enhanced expression of transforming growth factor-alpha (TGF-?) and glia maturation factor-beta (GMF-ß) correlate with severity of neuropathology in border disease virus-infected small ruminants
dc.typeArticle

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