Blaudschun R, Brenneisen P, Wlaschek M, Meewes C, Scharffetter-Kochanek K
Department of Dermatology, University of Cologne, Joseph-Stelzmann Str. 9, 50931, Cologne, Germany.
FEBS Lett. 2000 Jun 2;474(2-3):195-200. doi: 10.1016/s0014-5793(00)01605-7.
Ultraviolet B (UVB) irradiation, the major damaging component of sunlight, has earlier been reported to enhance cutaneous angiogenesis in chronically sun-exposed skin. We herein provide first evidence for a biphasic induction of the vascular endothelial growth factor (VEGF) following UVB irradiation of the human epidermal cell line HaCaT. The first VEGF peak occurred on mRNA level at 1 h and on protein level at 4 h postirradiation and is fully mediated by the UVB-dependent phosphorylation of the epidermal growth factor receptor, which subsequent to its phosphorylation also initiates at least in part the synthesis of transforming growth factor alpha that confers as shown previously the second late VEGF peak at 8 h on mRNA and at 24 h on protein level.
紫外线B（UVB）辐射是阳光中的主要损伤成分，此前有报道称其可增强长期暴露于阳光下皮肤的皮肤血管生成。我们在此首次提供了人类表皮细胞系HaCaT经UVB照射后血管内皮生长因子（VEGF）双相诱导的证据。第一个VEGF峰值在照射后1小时出现在mRNA水平，4小时出现在蛋白质水平，这完全由表皮生长因子受体的UVB依赖性磷酸化介导，该受体磷酸化后至少部分启动转化生长因子α的合成，如先前所示，其在mRNA水平8小时和蛋白质水平24小时产生第二个晚期VEGF峰值。
