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Dynamic distributions of tumor necrosis factor-alpha and its receptors in the red nucleus of rats with spared nerve injury.
Wang, Jing; Ding, Cui-Ping; Yu, Jing; Zeng, Xiao-Yan; Han, Shui-Ping; Wang, Jun-Yang.
Afiliación
  • Wang J; Departments of Pathogenic Biology and Immunology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
  • Ding CP; Departments of Pathogenic Biology and Immunology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
  • Yu J; Departments of Pathogenic Biology and Immunology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
  • Zeng XY; Department of Laboratory Medicine, The First Affiliated Hospital, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
  • Han SP; Department of Pathology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
  • Wang JY; Departments of Pathogenic Biology and Immunology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
Neuropathology ; 36(4): 346-53, 2016 Aug.
Article en En | MEDLINE | ID: mdl-26669937
Previous studies have demonstrated that tumor necrosis factor-alpha (TNF-α) in the red nucleus (RN) plays a facilitated role in the development of neuropathic pain, and its effect is transmitted through TNF-α receptor (TNFR) subtypes 1 and 2. Here, the dynamic distributions of TNF-α and TNFRs in the RN of rats with spared nerve injury (SNI) were investigated. Western blot analysis and immunofluorescence staining indicated that TNF-α was hardly expressed in the RN of normal rats but significantly increased at 1 week and peaked at 2 weeks after SNI. Neurons and oligodendrocytes showed TNF-α expression at both 1 week and 2 weeks after SNI, while astrocytes and microglia produced TNF-α later than neurons and oligodendrocytes starting at 2 weeks after SNI. TNFR1 was constitutively expressed in the RN of normal rats and significantly enhanced at 2 weeks but not 1 week after SNI; it was mainly localized in neurons, oligodendrocytes and microglia. Astrocytes were not immunopositive for TNFR1 under normal conditions and at 1 week after injury, but small amounts of astrocytes showed TNFR1 expression at 2 weeks after SNI. A low level of TNFR2 was expressed in the RN of normal rats, but it was significantly increased at 1 week and 2 weeks after SNI and localized in neurons and all three types of glia. These findings suggest that neurons and three types of glia in the RN all contribute to TNF-α production and participate in the initiation and/or maintenance of neuropathic pain induced by SNI. TNF-α exerts its effects in different types of cells maybe through different receptors, TNFR1 and/or TNFR2, in the different stages of neuropathic pain.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Núcleo Rojo / Factor de Necrosis Tumoral alfa / Receptores Tipo I de Factores de Necrosis Tumoral / Receptores Tipo II del Factor de Necrosis Tumoral / Neuralgia Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Neuropathology Asunto de la revista: NEUROLOGIA / PATOLOGIA Año: 2016 Tipo del documento: Article País de afiliación: China Pais de publicación: Australia
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Núcleo Rojo / Factor de Necrosis Tumoral alfa / Receptores Tipo I de Factores de Necrosis Tumoral / Receptores Tipo II del Factor de Necrosis Tumoral / Neuralgia Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Neuropathology Asunto de la revista: NEUROLOGIA / PATOLOGIA Año: 2016 Tipo del documento: Article País de afiliación: China Pais de publicación: Australia