Modulation of vascular endothelial growth factor receptors in melanocytes
Modulation of vascular endothelial growth factor receptors in melanocytes
复制标题
DOI：
10.1111/j.0906-6705.2005.00345.x
复制
发表时间：
2005-08-01
影响因子：
3.6
通讯作者：
Gilchrest, BA
中科院分区：
文献类型：
--
作者：
Kim, EJ;Park, HY;Gilchrest, BA
血管内皮生长因子（VEGF）是由角质形成细胞组成性产生的，但没有已知的表皮靶细胞。我们现在报告，正常人黑素细胞（MC）保持在无血清，激素，生长因子补充培养基缺乏佛波酯和choleragen组成型表达VEGF受体-1（VEGFR-1），VEGFR-2，和neuropilin-1。此外，用VEGF（165）同种型刺激Mc导致VEGFR-2的磷酸化，VEGFR-2是负责内皮细胞中大部分VEGF介导的效应的受体，表明该受体是功能性的。有趣的是，在Mc中，VEGFR-2表达由紫外线照射诱导，并被VEGF和肿瘤坏死因子-α下调。在佛波醇酯存在下的延长培养（> 8周）消除了VEGFR-2表达，解释了先前报道的Mc不表达VEGFR-1和VEGFR-2。这些数据表明，VEGF可能在皮肤中的Mc行为中发挥作用。
Vascular endothelial growth factor (VEGF) is constitutively produced by keratinocytes, but has no known epidermal target cell. We now report that normal human melanocytes (Mc) maintained in serum-free, hormone-, and growth factor-supplemented medium lacking phorbol ester and choleragen constitutively express VEGF receptor-1 (VEGFR-1), VEGFR-2, and neuropilin-1. Furthermore, stimulation of Mc with VEGF(165) isoform leads to phosphorylation of VEGFR-2, the receptor responsible for most of the VEGF-mediated effects in endothelial cells, suggesting that the receptor is functional. Interestingly, in Mc, VEGFR-2 expression is induced by ultraviolet irradiation and is downregulated by VEGF and tumor necrosis factor-alpha. Prolonged culture (> 8 weeks) in the presence of phorbol ester abrogates VEGFR-2 expression, explaining previous reports that Mc do not express VEGFR-1 and VEGFR-2. These data suggest that VEGF may play a role in Mc behavior in skin.