Your browser doesn't support javascript.
loading
Cbl-b deficiency provides protection against UVB-induced skin damage by modulating inflammatory gene signature.
Singh, Tej Pratap; Vieyra-Garcia, Pablo A; Wagner, Karin; Penninger, Josef; Wolf, Peter.
Afiliación
  • Singh TP; Research Unit for Photodermatology, Department of Dermatology and Venereology, Medical University of Graz, Graz, Austria.
  • Vieyra-Garcia PA; Center for Medical Research, Medical University of Graz, Graz, Austria.
  • Wagner K; Inflammation Biology Section, Laboratory of Molecular Immunology, NIAID, NIH, Building 10, Room 11N112, 10 Center Drive, Bethesda, MD, 20892, USA.
  • Penninger J; Research Unit for Photodermatology, Department of Dermatology and Venereology, Medical University of Graz, Graz, Austria.
  • Wolf P; Center for Medical Research, Medical University of Graz, Graz, Austria.
Cell Death Dis ; 9(8): 835, 2018 08 06.
Article en En | MEDLINE | ID: mdl-30082827
Exposure of skin to ultraviolet (UV) radiation induces DNA damage, inflammation, and immune suppression that ultimately lead to skin cancer. However, some of the pathways that regulate these events are poorly understood. We exposed mice to UVB to study its early effects in the absence of Cbl-b, a known suppressor of antitumor immune response in the skin. Cbl-b-/- mice were protected from UV-induced cell damage as shown by the lower number of cyclobutane pyrimidine dimers and sunburn cells in exposed skin compared to wild-type mice. Microarray data revealed that deficiency of Cbl-b resulted in differential expression of genes involved in apoptosis evasion, tumor suppression and cell survival in UV-exposed skin. After UVB, Cbl-b-/- mice upregulated gene expression pattern associated with regulation of epidermal cell proliferation linked to Wnt signaling mediators and enzymes that relate to cell removal and tissue remodeling like MMP12. Additionally, the skin of Cbl-b-/- mice was protected from chronic inflammatory responses and epidermal hyperplasia in a 4-weeks UVB treatment protocol. Overall, our results suggest a novel role for Cbl-b in regulating inflammation and physiologic clearance of damaged cells in response to UVB by modulating inflammatory gene signature.
Asunto(s)
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Piel / Rayos Ultravioleta / Proteínas Adaptadoras Transductoras de Señales / Proteínas Proto-Oncogénicas c-cbl Tipo de estudio: Guideline Límite: Animals Idioma: En Revista: Cell Death Dis Año: 2018 Tipo del documento: Article País de afiliación: Austria Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Piel / Rayos Ultravioleta / Proteínas Adaptadoras Transductoras de Señales / Proteínas Proto-Oncogénicas c-cbl Tipo de estudio: Guideline Límite: Animals Idioma: En Revista: Cell Death Dis Año: 2018 Tipo del documento: Article País de afiliación: Austria Pais de publicación: Reino Unido