Por favor, use este identificador para citar o enlazar este ítem: 10.14670/HH-11-621

Título: eNOS and iNOS trigger apoptosis in the brains of sheep and goats naturally infected with the border disease virus
Fecha de publicación: 2015
Editorial: F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología
Cita bibliográfica: Histology and histopathology, Vol. 30, nº10, (2015)
ISSN: 1699-5848
0213-3911
Materias relacionadas: CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología
Palabras clave: Apoptosis
Border disease
eNOS
iNOS
Resumen: In this study, apoptotic and anti-apoptotic mechanisms and if present, which pathway to trigger the apoptosis in the brains of Border Disease Virus (BDV) infected lambs (n=10) and goat kids (n=5) were investigated. Briefly, apoptotic (caspase 3, caspase 9) and anti-apoptotic markers (Bcl-2), cytokine response (TNF-α, INF-γ), reactive gliosis and myelin loss were examined. eNOS, iNOS, caspase 9, caspase 3 and GFAP expressions were higher in BDV infected tissues compared to control animals (6 kids and 6 lambs) (p<0.05). Double immunoperoxidase test revelaed that TUNEL positive apoptotic cells showed significant association with increased eNOS-iNOS and iNOS-BDV expressions. However, no significant differences were found for TNFR1, TNF-α and INF-γ expressions in BD (p>0.05). There was a positive correlation between the intensity of myelin loss, GFAP activity and severity of infection. Inconclusion, as a novel finding, it is established that eNOS and iNOS overexpressions are coassociated with apoptosis in BDV infected neurons and neuroglia. The results also strongly suggested that BDV infected apoptotic cells mainly prefer the intrinsic pathway that might be most likely related to increased nitric oxide levels.
Autor/es principal/es: Cagdas Dince, Gungor
Kul, Oguz
URI: http://hdl.handle.net/10201/99808
DOI: 10.14670/HH-11-621
Tipo de documento: info:eu-repo/semantics/article
Número páginas / Extensión: 10
Derechos: info:eu-repo/semantics/openAccess
Attribution-NonCommercial-NoDerivatives 4.0 International
Aparece en las colecciones:Vol.30,nº10 (2015)

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