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Blood, 15 March 2005, Vol. 105, No. 6, pp. 2392-2399.
Prepublished online as a Blood First Edition Paper on November 18, 2004; DOI 10.1182/blood-2004-06-2435.
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Submitted June 28, 2004
Accepted November 16, 2004
Vascular endothelial growth factor promotes sensitivity to ultraviolet-B-induced cutaneous photodamage
Satoshi Hirakawa, Seishiro Fujii, Kentaro Kajiya, Kiichiro Yano, and Michael Detmar*
Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA
Shiseido Life Science Research Center, Yokohama, Japan
Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA; Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland
* Corresponding author; email: michael.detmar{at}pharma.ethz.ch.
Acute ultraviolet B (UVB) irradiation of the skin results in erythema, vasodilation, edema and angiogenesis, which is associated with the expression of vascular endothelial growth factor (VEGF) by epidermal keratinocytes. It is not clear, however, if VEGF is required for the damage and/or repair process that occurs in the skin upon UVB exposure. We subjected transgenic mice that overexpress VEGF, and their wild-type littermates, to graded doses of acute UVB irradiation. The skin of VEGF overexpressing mice was highly photosensitive, and became erythematic when exposed to half the UVB dose required to induce erythema in wild-type mice. Erythema was associated with proliferation of dermal endothelial cells, cutaneous edema, and inflammatory cell infiltration. When mice were subjected to 10 weeks of low-level UVB irradiation, no major changes were observed in wild-type mice, whereas VEGF transgenic mice developed skin damage with degradation of the dermal matrix and enhanced vascularization. Systemic treatment with an anti-VEGF blocking antibody reduced the sensitivity of wild-type mice to acute UVB irradiation, without inhibiting post-UVB repair. Our results reveal that VEGF promotes the cutaneous damage that occurs after UVB exposure, and that the VEGF signaling pathway might serve as a novel target for the prevention of UVB-induced photodamage.
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