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1例Langer-Saldino软骨发育不全病例中透明软骨II型胶原蛋白的缺失及蛋白聚糖结构的改变

The absence of type II collagen and changes in proteoglycan structure of hyaline cartilage in a case of Langer-Saldino achondrogenesis.

作者信息

Feshchenko S P, Rebrin I A, Sokolnik V P, Sher B M, Sokolov B P, Kalinin V N, Lazjuk G I

机构信息

Byelorussian Institute for Hereditary Disease, Minsk, USSR.

出版信息

Hum Genet. 1989 Apr;82(1):49-54. doi: 10.1007/BF00288271.

Abstract

Structural analysis of hyaline cartilage extracellular matrix components from the ribs and knee joint of a stillborn female with type II achondrogenesis was carried out. The absence of type II collagen, a decrease in the amount of proteoglycans (PG), and structural changes in PG, namely, increased electrophoretic mobility of PG, lower relative content of chondroitin 4-sulfate (Ch4-S), lower molecular weight and decreased total chondroitin sulfate (ChS) sulfation, were detected. Increased amounts of type I and type III collagens, atypical for hyaline cartilage, were revealed. Among the link proteins (LPs), a large protein with a mol. wt. of 48 kDa was predominant. Molecular and cellular mechanisms of the pathogenesis of achondrogenesis ("chondrogenesis imperfecta") are discussed. The data obtained suggest that the primary defect in type II achondrogenesis involves ChS or type II collagen synthesis.

摘要

对一名患有II型软骨发育不全的死产女婴的肋骨和膝关节透明软骨细胞外基质成分进行了结构分析。检测到II型胶原蛋白缺失、蛋白聚糖(PG)数量减少以及PG的结构变化,即PG的电泳迁移率增加、硫酸软骨素4-硫酸盐(Ch4-S)的相对含量降低、分子量降低以及总硫酸软骨素(ChS)硫酸化减少。还发现了透明软骨中不典型的I型和III型胶原蛋白数量增加。在连接蛋白(LP)中,一种分子量为48 kDa的大蛋白占主导地位。讨论了软骨发育不全(“软骨发育不全”)发病机制的分子和细胞机制。获得的数据表明,II型软骨发育不全的主要缺陷涉及ChS或II型胶原蛋白的合成。

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