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Modulation of vascular endothelial growth factor receptors in melanocytes
Author(s) -
Kim Ellen J.,
Park HeeYoung,
Yaar Mina,
Gilchrest Barbara A.
Publication year - 2005
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.0906-6705.2005.00345.x
Subject(s) - vascular endothelial growth factor , receptor , neuropilin 1 , endocrinology , medicine , kinase insert domain receptor , epidermal growth factor , cancer research , vascular endothelial growth factor a , growth factor receptor inhibitor , biology , growth factor , chemistry , microbiology and biotechnology , vegf receptors
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‐α. 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.