Clinique Vétérinaire, Cidex 248, R. N. 85, 06330-Roquefort les Pins, France.
College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough street, Raleigh, NC 27606, USA.
Vet Dermatol. 1999 Mar;10(1):3-16. doi: 10.1046/j.1365-3164.1999.00132.x.
Murine models recently provided important information on the pathogenesis of pigmentation disorders. Multiple factors influence melanocyte function at various levels, such as melanoblast development and migration from the neural crest to peripheral sites, melanoblast differentiation into melanocytes, melanocyte survival and, finally, synthesis of melanosomes and melanins. Mutations affecting any of these steps result in hereditary hypomelanoses. In some of these diseases, melanocytes are absent, either because of a defect in migration of melanoblasts from the neural crest, their inability to survive and/or proliferate in colonized territories (piebaldism and Waardenburg syndromes), or because of programmed melanocyte destruction (e.g. vitiligo). In other entities, the melanocytes are present but functionally deficient (oculocutaneous albinisms and pigmentary dilutions). This comprehensive review will introduce the genetic regulation of melanocytogenesis and melanogenesis and the correlations between genetic abnormalities and hypopigmentation clinical disorders.
小鼠模型最近为色素沉着障碍的发病机制提供了重要信息。多种因素在不同水平影响黑素细胞功能,如黑素母细胞的发育以及从神经嵴向周边部位的迁移、黑素母细胞分化为黑素细胞、黑素细胞存活,最后是黑素小体和黑色素的合成。影响这些步骤中任何一步的突变都会导致遗传性色素减退。在其中一些疾病中,黑素细胞缺失,这要么是由于黑素母细胞从神经嵴迁移存在缺陷,它们无法在定植区域存活和/或增殖(斑驳病和瓦登伯革综合征),要么是由于黑素细胞的程序性破坏(如白癜风)。在其他疾病中,黑素细胞存在但功能缺陷(眼皮肤白化病和色素稀释)。这篇综述将介绍黑素细胞生成和黑素生成的遗传调控以及基因异常与色素减退临床疾病之间的相关性。