z-logo
Premium
Expression and function of neurotrophins and their receptors in human melanocytes
Author(s) -
Marconi A.,
Panza M. C.,
BonnetDuquennoy M.,
Lazou K.,
Kurfurst R.,
Truzzi F.,
Lotti R.,
De Santis G.,
Dumas M.,
Bonté F.,
Pincelli C.
Publication year - 2006
Publication title -
international journal of cosmetic science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.532
H-Index - 62
eISSN - 1468-2494
pISSN - 0142-5463
DOI - 10.1111/j.1467-2494.2006.00321.x
Subject(s) - melanocyte , neurotrophin , nerve growth factor , tropomyosin receptor kinase a , receptor , neurotrophic factors , biology , tyrosinase , neurotrophin 3 , endocrinology , tropomyosin receptor kinase b , downregulation and upregulation , microbiology and biotechnology , medicine , trk receptor , phorbol , brain derived neurotrophic factor , signal transduction , melanoma , cancer research , protein kinase c , biochemistry , enzyme , gene
Synopsis Melanocytes and cells of the nervous system are of common ectodermal origin and neurotrophins (NT) have been shown to be released by human keratinocytes. We investigated the expression and function of NT [nerve growth factor (NGF), brain‐derived neurotrophic factor (BDNF), NT‐3, NT‐4/‐5] and their receptors in human melanocytes. Human melanocytes produce all NT in different amounts, whereas they only release NT‐4. NT‐4 release is downregulated, whereas NT‐3 is upregulated by ultraviolet (UVB) irradiation. Melanocytes treated with phorbol 12‐myristate 13‐acetate (PMA) express TrkA and TrkB, but not TrkC. NT fail to stimulate melanocyte proliferation, whereas they stimulate the synthesis of tyrosinase and tyrosinase‐related protein‐1 (TRP‐1). Finally, NT‐3, NT‐4 and NGF increase melanin production. Taken together, these results demonstrate an intriguing interaction between melanocytes and the nervous system. We speculate that NT could be considered the target of therapy for disorders of skin pigmentation.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here