Talk:Integumentary System Development: Difference between revisions

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Pigment Cell Melanoma Res. 2008 Dec;21(6):598-610. Review.
Pigment Cell Melanoma Res. 2008 Dec;21(6):598-610. Review.
PMID: 19067969
PMID: 19067969
===Two distinct types of mouse melanocyte: differential signaling requirement for the maintenance of non-cutaneous and dermal versus epidermal melanocytes===
Development. 2009 Aug;136(15):2511-21. Epub 2009 Jun 24.
Aoki H, Yamada Y, Hara A, Kunisada T.
Department of Tissue and Organ Development, Regeneration, and Advanced Medical Science, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan.
Abstract
Unlike the thoroughly investigated melanocyte population in the hair follicle of the epidermis, the growth and differentiation requirements of the melanocytes in the eye, harderian gland and inner ear - the so-called non-cutaneous melanocytes - remain unclear. In this study, we investigated the in vitro and in vivo effects of the factors that regulate melanocyte development on the stem cells or the precursors of these non-cutaneous melanocytes. In general, a reduction in KIT receptor tyrosine kinase signaling leads to disordered melanocyte development. However, melanocytes in the eye, ear and harderian gland were revealed to be less sensitive to KIT signaling than cutaneous melanocytes. Instead, melanocytes in the eye and harderian gland were stimulated more effectively by endothelin 3 (ET3) or hepatocyte growth factor (HGF) signals than by KIT signaling, and the precursors of these melanocytes expressed the lowest amount of KIT. The growth and differentiation of these non-cutaneous melanocytes were specifically inhibited by antagonists for ET3 and HGF. In transgenic mice induced to express ET3 or HGF in their skin and epithelial tissues from human cytokeratin 14 promoters, the survival and differentiation of non-cutaneous and dermal melanocytes, but not epidermal melanocytes, were enhanced, apparently irrespective of KIT signaling. These results provide a molecular basis for the clear discrimination between non-cutaneous or dermal melanocytes and epidermal melanocytes, a difference that might be important in the pathogenesis of melanocyte-related diseases and melanomas.
PMID: 19553284 http://www.ncbi.nlm.nih.gov/pubmed/19553284

Revision as of 19:21, 30 September 2010

Biology and Genetics of Hair. http://www.ncbi.nlm.nih.gov/pubmed/20590427


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2064709/?tool=pubmed


Melanoblasts

Ex vivo live imaging of melanoblast migration in embryonic mouse skin.

Pigment Cell Melanoma Res. 2010 Apr;23(2):299-301. Epub 2010 Jan 7.

Mort RL, Hay L, Jackson IJ.

PMID: 20067551 http://www.ncbi.nlm.nih.gov/pubmed/20067551

Melanoblasts are the embryonic precursors of melanocytes. They are derived from the neural crest at around embryonic day 9.5 (E9.5) and upregulate early melanoblast specific markers (Mitf, Tyrosinase, Dct, Kit) around E10.5.


Includes videos of melanoblast migration in model mouse skin system.

The making of a melanocyte: the specification of melanoblasts from the neural crest.

Thomas AJ, Erickson CA. Pigment Cell Melanoma Res. 2008 Dec;21(6):598-610. Review. PMID: 19067969


Two distinct types of mouse melanocyte: differential signaling requirement for the maintenance of non-cutaneous and dermal versus epidermal melanocytes

Development. 2009 Aug;136(15):2511-21. Epub 2009 Jun 24.

Aoki H, Yamada Y, Hara A, Kunisada T.

Department of Tissue and Organ Development, Regeneration, and Advanced Medical Science, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan. Abstract Unlike the thoroughly investigated melanocyte population in the hair follicle of the epidermis, the growth and differentiation requirements of the melanocytes in the eye, harderian gland and inner ear - the so-called non-cutaneous melanocytes - remain unclear. In this study, we investigated the in vitro and in vivo effects of the factors that regulate melanocyte development on the stem cells or the precursors of these non-cutaneous melanocytes. In general, a reduction in KIT receptor tyrosine kinase signaling leads to disordered melanocyte development. However, melanocytes in the eye, ear and harderian gland were revealed to be less sensitive to KIT signaling than cutaneous melanocytes. Instead, melanocytes in the eye and harderian gland were stimulated more effectively by endothelin 3 (ET3) or hepatocyte growth factor (HGF) signals than by KIT signaling, and the precursors of these melanocytes expressed the lowest amount of KIT. The growth and differentiation of these non-cutaneous melanocytes were specifically inhibited by antagonists for ET3 and HGF. In transgenic mice induced to express ET3 or HGF in their skin and epithelial tissues from human cytokeratin 14 promoters, the survival and differentiation of non-cutaneous and dermal melanocytes, but not epidermal melanocytes, were enhanced, apparently irrespective of KIT signaling. These results provide a molecular basis for the clear discrimination between non-cutaneous or dermal melanocytes and epidermal melanocytes, a difference that might be important in the pathogenesis of melanocyte-related diseases and melanomas.

PMID: 19553284 http://www.ncbi.nlm.nih.gov/pubmed/19553284