Nusgens B V, Verellen-Dumoulin C, Hermanns-Lê T, De Paepe A, Nuytinck L, Piérard G E, Lapière C M
Laboratory of Experimental Dermatology, Tour de Patholgie, Sart, Belgium.
Nat Genet. 1992 Jun;1(3):214-7. doi: 10.1038/ng0692-214.
Ehlers-Danlos (ED) syndrome type VII is characterized by the accumulation of collagen precursors in connective tissues. ED VII A and B are caused by mutations in the genes of alpha 1 and alpha 2 collagen I which result in the disruption of the cleavage site of procollagen I N-proteinase. The existence of ED VII C in humans has been hypothesized on the basis of a disorder in cattle and sheep related to the absence of the enzyme. We now present evidence for the existence of this disease in humans, characterized by skin fragility, altered polymers seen as hieroglyphic pictures with electron microscopy, accumulation of p-N-alpha 1 and p-N-alpha 2 collagen type I in the dermis and absence of processing of the p-N-I polypeptides in fibroblast cultures.
VII型埃勒斯-当洛综合征(Ehlers-Danlos,ED)的特征是结缔组织中胶原蛋白前体的积累。ED VII A和B是由α1和α2 I型胶原蛋白基因突变引起的,这些突变导致I型前胶原N蛋白酶切割位点的破坏。基于牛和羊中与该酶缺失相关的一种疾病,人们推测人类中存在ED VII C。我们现在提供了人类中存在这种疾病的证据,其特征为皮肤脆弱、电子显微镜下呈现象形图片的改变聚合物、真皮中I型p-N-α1和p-N-α2胶原蛋白的积累以及成纤维细胞培养中p-N-I多肽缺乏加工。