Ultraviolet B irradiation of human skin induces an angiogenic switch that is mediated by upregulation of vascular endothelial growth factor and by downregulation of thrombospondin-1.
Br J Dermatol
; 152(1): 115-21, 2005 Jan.
Article
en En
| MEDLINE
| ID: mdl-15656811
ABSTRACT
BACKGROUND:
We have previously demonstrated that skin-specific overexpression of the endogenous angiogenesis inhibitor thrombospondin (TSP)-1 prevented chronic ultraviolet (UV) B-induced angiogenesis, inflammatory cell infiltration and cutaneous photodamage in mice.OBJECTIVES:
To elucidate the mechanisms by which acute UVB-induced angiogenesis induces dermal damage, and to study the molecular regulation of acute UVB-induced angiogenesis in human skin.METHODS:
We subjected five healthy volunteers to acute UVB irradiation (2 minimal erythema doses) and performed histological analysis at 48 h after UVB irradiation.RESULTS:
Histology revealed epidermal hyperplasia, infiltration of elastase-producing neutrophils and elastin fibre damage. Immunohistochemistry for CD31 demonstrated pronounced angiogenesis with a significant increase in both vascular density and vessel size, associated with increased endothelial cell proliferation. Whereas constitutive expression of TSP-1 but only weak expression of vascular endothelial growth factor (VEGF) were detected in normal human epidermis, pronounced downregulation of TSP-1 and upregulation of VEGF were observed in epidermal keratinocytes after acute UVB irradiation. These findings were confirmed by quantitative reverse transcription-polymerase chain reaction analysis after UVB irradiation of cultured HaCaT keratinocytes in vitro.CONCLUSIONS:
Together, these data indicate that a disruption of the balance between VEGF and TSP-1 expression leads to a UVB-induced angiogenic switch, facilitating the infiltration of elastase-producing leucocytes and cutaneous photodamage.
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Base de datos:
MEDLINE
Asunto principal:
Piel
/
Rayos Ultravioleta
/
Trombospondina 1
/
Factor A de Crecimiento Endotelial Vascular
/
Neovascularización Patológica
Tipo de estudio:
Etiology_studies
Límite:
Adult
/
Humans
/
Middle aged
Idioma:
En
Revista:
Br J Dermatol
Año:
2005
Tipo del documento:
Article
País de afiliación:
Japón