Expression and function of neurotrophins and their receptors in human melanocytes
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] an...
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Published in | International journal of cosmetic science Vol. 28; no. 4; pp. 255 - 261 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.08.2006
Blackwell Science |
Subjects | |
Online Access | Get full text |
ISSN | 0142-5463 1468-2494 1468-2494 1467-2494 |
DOI | 10.1111/j.1467-2494.2006.00321.x |
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Abstract | 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.
Résumé
Les melanocytes et le système nerveux central ont en commun une origine ectodermique et les neurotrophines (NT) sont connues pour etre libérées par les kératinocytes. Dans la présente étude nous décrivons l'expression, la fonction des neurotrophines et leurs récepteurs chez les mélanocytes humains normaux. Les mélanocytes produisent toutes les NT en différentes quantités, mais ne libèrent que la NT‐4. L'irradiation UVB decroit la production de NT‐4 et stimule celle de NT‐3. Les mélanocytes traités au PMA expriment TrkA et TrkB mais pas TrkC. Les Neurotrophines stimulent pas la prolifération des mélanocytes mais stimulent la synthèse de la tyrosinase et de la TRP‐1. Finallement, NT‐3, NT‐4 et le NGF augmentent la production de mélanine. L ’ensemble de ces résultats démontrent une interaction entre le système nerveux et les mélanocytes. Nous émettons l'hypothèse que les NT doivent etre considérées comme des cibles sérieuses pour la correction des désordres de pigmentation cutanée. |
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AbstractList | 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.Original Abstract: Les melanocytes et le systeme nerveux central ont en commun une origine ectodermique et les neurotrophines (NT) sont connues pour etre liberees par les keratinocytes. Dans la presente etude nous decrivons l'expression, la fonction des neurotrophines et leurs recepteurs chez les melanocytes humains normaux. Les melanocytes produisent toutes les NT en differentes quantites, mais ne liberent que la NT-4. L'irradiation UVB decroit la production de NT-4 et stimule celle de NT-3. Les melanocytes traites au PMA expriment TrkA et TrkB mais pas TrkC. Les Neurotrophines stimulent pas la proliferation des melanocytes mais stimulent la synthese de la tyrosinase et de la TRP-1. Finallement, NT-3, NT-4 et le NGF augmentent la production de melanine. L 'ensemble de ces resultats demontrent une interaction entre le systeme nerveux et les melanocytes. Nous emettons l'hypothese que les NT doivent etre considerees comme des cibles serieuses pour la correction des desordres de pigmentation cutanee. 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.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. 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. 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. Résumé Les melanocytes et le système nerveux central ont en commun une origine ectodermique et les neurotrophines (NT) sont connues pour etre libérées par les kératinocytes. Dans la présente étude nous décrivons l'expression, la fonction des neurotrophines et leurs récepteurs chez les mélanocytes humains normaux. Les mélanocytes produisent toutes les NT en différentes quantités, mais ne libèrent que la NT‐4. L'irradiation UVB decroit la production de NT‐4 et stimule celle de NT‐3. Les mélanocytes traités au PMA expriment TrkA et TrkB mais pas TrkC. Les Neurotrophines stimulent pas la prolifération des mélanocytes mais stimulent la synthèse de la tyrosinase et de la TRP‐1. Finallement, NT‐3, NT‐4 et le NGF augmentent la production de mélanine. L ’ensemble de ces résultats démontrent une interaction entre le système nerveux et les mélanocytes. Nous émettons l'hypothèse que les NT doivent etre considérées comme des cibles sérieuses pour la correction des désordres de pigmentation cutanée. 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. Les melanocytes et le système nerveux central ont en commun une origine ectodermique et les neurotrophines (NT) sont connues pour etre libérées par les kératinocytes. Dans la présente étude nous décrivons l'expression, la fonction des neurotrophines et leurs récepteurs chez les mélanocytes humains normaux. Les mélanocytes produisent toutes les NT en différentes quantités, mais ne libèrent que la NT‐4. L'irradiation UVB decroit la production de NT‐4 et stimule celle de NT‐3. Les mélanocytes traités au PMA expriment TrkA et TrkB mais pas TrkC. Les Neurotrophines stimulent pas la prolifération des mélanocytes mais stimulent la synthèse de la tyrosinase et de la TRP‐1. Finallement, NT‐3, NT‐4 et le NGF augmentent la production de mélanine. L ’ensemble de ces résultats démontrent une interaction entre le système nerveux et les mélanocytes. Nous émettons l'hypothèse que les NT doivent etre considérées comme des cibles sérieuses pour la correction des désordres de pigmentation cutanée. |
Author | Truzzi, F. Kurfurst, R. Lotti, R. Pincelli, C. Marconi, A. Lazou, K. Panza, M. C. De Santis, G. Bonté, F. Bonnet-Duquennoy, M. Dumas, M. |
Author_xml | – sequence: 1 givenname: A. surname: Marconi fullname: Marconi, A. organization: Institute of Dermatology and Plastic Surgery Unit, University of Modena and Reggio Emilia, 41100 Modena, Italy – sequence: 2 givenname: M. C. surname: Panza fullname: Panza, M. C. organization: Institute of Dermatology and Plastic Surgery Unit, University of Modena and Reggio Emilia, 41100 Modena, Italy – sequence: 3 givenname: M. surname: Bonnet-Duquennoy fullname: Bonnet-Duquennoy, M. organization: LVMH Recherche, 45804 Saint Jean de Braye, France – sequence: 4 givenname: K. surname: Lazou fullname: Lazou, K. organization: Institute of Dermatology and Plastic Surgery Unit, University of Modena and Reggio Emilia, 41100 Modena, Italy – sequence: 5 givenname: R. surname: Kurfurst fullname: Kurfurst, R. organization: LVMH Recherche, 45804 Saint Jean de Braye, France – sequence: 6 givenname: F. surname: Truzzi fullname: Truzzi, F. organization: Institute of Dermatology and Plastic Surgery Unit, University of Modena and Reggio Emilia, 41100 Modena, Italy – sequence: 7 givenname: R. surname: Lotti fullname: Lotti, R. organization: Institute of Dermatology and Plastic Surgery Unit, University of Modena and Reggio Emilia, 41100 Modena, Italy – sequence: 8 givenname: G. surname: De Santis fullname: De Santis, G. organization: Institute of Dermatology and Plastic Surgery Unit, University of Modena and Reggio Emilia, 41100 Modena, Italy – sequence: 9 givenname: M. surname: Dumas fullname: Dumas, M. organization: LVMH Recherche, 45804 Saint Jean de Braye, France – sequence: 10 givenname: F. surname: Bonté fullname: Bonté, F. organization: LVMH Recherche, 45804 Saint Jean de Braye, France – sequence: 11 givenname: C. surname: Pincelli fullname: Pincelli, C. organization: Institute of Dermatology and Plastic Surgery Unit, University of Modena and Reggio Emilia, 41100 Modena, Italy |
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Keywords | Human Neurotrophin Ultraviolet radiation Regulation(control) UVB radiation Melanocyte neurotrophin receptor Melanogenesis Gene expression Protein Biological receptor |
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References_xml | – reference: Hallbook, F., Ibanez, C.F. and Persson H. Evolutionary studies of the nerve growth factor family reveal a novel member abundantly expressed in Xenopus ovary. Neuron 6, 845-858 (1991). – reference: Chao, M.V., Bothwell, M.A., Ross, A.H. et al. Gene transfer and molecular cloning of the human NGF receptor. Science 232, 518-521 (1986). – reference: Hohn, A., Leibrock, J., Bailey, K. and Barde, Y.A. Identification and characterization of a novel member of the nerve growth factor/brain-derived neurotrophic factor family. Nature 344, 339-341 (1990). – reference: Pincelli, C., Fantini, F. and Giannetti, A. Nerve growth factor and the skin. Int. J. Dermatol. 33, 308-312 (1994). – reference: Grando, S.A., Cabrera, R., Hostager, B.S. et al. Computerized microassay of keratinocyte cell-plastic attachment and proliferation for assessing net stimulatory, inhibitory and toxic effects of compounds on nonimmortalized cell lines. 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Melanocytes and cells of the nervous system are of common ectodermal origin and neurotrophins (NT) have been shown to be released by human... 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... Synopsis: Melanocytes and cells of the nervous system are of common ectodermal origin and neurotrophins (NT) have been shown to be released by human... |
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SubjectTerms | Biological and medical sciences Fundamental and applied biological sciences. Psychology melanocyte melanogenesis neurotrophin receptor ultraviolet radiation Vertebrates: skin, associated glands, phaneres, light organs, various exocrine glands (salt gland, uropygial gland...), adipose tissue, connective tissue |
Title | Expression and function of neurotrophins and their receptors in human melanocytes |
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