Chronic ultraviolet B (UVB) irradiation (290–320 nm) of the skin results in the degradation of extracellular matrix macromolecules,
elastosis, formation of wrinkles [
[1]
] and enhanced risk for skin cancer [
[2]
]. We have previously found that chronic UVB irradiation of human and mouse skin induces
pronounced angiogenesis of cutaneous blood vessels [
3
,
4
]. Moreover, targeted overexpression of vascular endothelial growth factor (VEGF)-A
enhanced the sensitivity to UVB-induced cutaneous photodamage [
[5]
], whereas transgenic overexpression of the angiogenesis inhibitor thrombospondin-1
in the epidermis completely prevented UVB-induced skin damage [
[3]
]. Together, these findings indicate that the cutaneous blood vasculature plays a critical
role in the mediation of photodamage. In contrast, the role of cutaneous lymphatic
vessels in the response to UVB irradiation has remained unknown.Keywords
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References
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Article Info
Publication History
Received:
February 15,
2007
Identification
Copyright
© 2007 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.
