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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. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-06-2435v1 105/6/2392    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Hirakawa, S. Articles by Detmar, M. Search for Related Content PubMed PubMed Citation Articles by Hirakawa, S. Articles by Detmar, M. Related Collections Hemostasis, Thrombosis, and Vascular Biology Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Vascular endothelial growth factor promotes sensitivity to ultraviolet B–induced cutaneous photodamage Satoshi Hirakawa, Seishiro Fujii, Kentaro Kajiya, Kiichiro Yano, and Michael Detmar From the Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA; the Shiseido Life Science Research Center, Yokohama, Japan; and the Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, Zurich, Switzerland. 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 unclear, however, whether VEGF is required for the damage or repair process that occurs in the skin on 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 proliferating dermal endothelial cells, cutaneous edema, and inflammatory cell infiltration. When 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 associated 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: VEGF, sunburn, and wrinkles Stephen C. Ekker Blood 2005 105: 2246. [Full Text] [PDF] This article has been cited by other articles: C. Halin, H. Fahrngruber, J. G. Meingassner, G. Bold, A. Littlewood-Evans, A. Stuetz, and M. Detmar Inhibition of Chronic and Acute Skin Inflammation by Treatment with a Vascular Endothelial Growth Factor Receptor Tyrosine Kinase Inhibitor Am. J. Pathol., July 1, 2008; 173(1): 265 - 277. [Abstract] [Full Text] [PDF] Minerva BMJ, March 19, 2005; 330(7492): 680 - 680. [Full Text] [PDF]

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