Tajima S, Takehana M, Azuma N
Department of Dermatology, Keio University School of Medicine, Tokyo, Japan.
J Dermatol. 1994 Apr;21(4):219-22. doi: 10.1111/j.1346-8138.1994.tb01726.x.
Collagen synthesis in cultured skin fibroblasts from a patient with osteogenesis imperfecta was studied. Approximately 2 fold accumulation of collagen in the cell layer was found. The slower mobility of pro alpha 1 (I) and pro alpha 2 (I) as well as alpha 1 and alpha 2 (I) polypeptide on sodium dodecylsulfate-polyacrylamide gel electrophoresis was detected, indicating that abnormal posttranslational modification could be present in type I procollagen in patient fibroblasts. The degrees of hydroxylation and subsequent glycosylation of lysine residues in the affected collagen were elevated 1.5 and 1.4 fold, respectively. There were no significant changes in the relative content of type III to type I collagen nor the incorporation of mannose into the carboxyterminal propeptide of pro alpha 1 (I) and pro alpha 2 (I). These results indicate that the patient produces an over-modified type I procollagen which is responsible for the clinical features and has a collagen abnormality already reported in type II osteogenesis imperfecta.
对一名成骨不全患者培养的皮肤成纤维细胞中的胶原蛋白合成进行了研究。发现细胞层中胶原蛋白积累约2倍。在十二烷基硫酸钠-聚丙烯酰胺凝胶电泳上检测到前α1(I)和前α2(I)以及α1和α2(I)多肽的迁移速度较慢,表明患者成纤维细胞中的I型前胶原可能存在异常的翻译后修饰。受影响胶原蛋白中赖氨酸残基的羟基化程度和随后的糖基化程度分别提高了1.5倍和1.4倍。III型与I型胶原蛋白的相对含量以及甘露糖掺入前α1(I)和前α2(I)的羧基末端前肽中均无显著变化。这些结果表明,该患者产生了过度修饰的I型前胶原,这导致了临床特征,并且具有已在II型成骨不全中报道的胶原蛋白异常。