Quantock A J, Meek K M, Fullwood N J, Zabel R W
Biophysics Group, Open University, Oxford Research Unit.
Can J Ophthalmol. 1993 Oct;28(6):266-72.
Processes that modulate the regular architecture and, hence, transparency of the cornea are poorly understood, although proteoglycans are thought to be involved. Scheie's syndrome displays corneal opacification and systemic accumulation of glycosaminoglycans. The manifestations of these two occurrences were examined in relation to the corneal stroma. Collagen architecture was investigated by transmission electron microscopy and synchroton x-ray diffraction. Cuprolinic blue staining located sulfated glycosaminoglycan deposits that disrupted the extracellular matrix. Unlike normal cornea, which contained collagen fibrils of remarkably uniform diameter (26.0 +/- 2.4 nm), there was a large range of fibril sizes in the Scheie's syndrome stroma (19.9 to 52.0 nm). Moreover, the distribution of fibril diameters appeared bimodal. X-ray diffraction confirmed the discovery of abnormally large stromal collagen. The results suggest a link in Scheie's syndrome between proteoglycan content/distribution and stromal disruption, and between stromal disruption and corneal opacification.
尽管人们认为蛋白聚糖参与其中,但调节角膜正常结构及透明度的过程仍鲜为人知。施艾氏综合征表现为角膜混浊和糖胺聚糖的全身蓄积。针对这两种情况的表现,研究人员结合角膜基质进行了检查。通过透射电子显微镜和同步加速器X射线衍射研究了胶原结构。铜啉蓝染色定位了破坏细胞外基质的硫酸化糖胺聚糖沉积物。正常角膜含有直径非常均匀(26.0±2.4纳米)的胶原纤维,与之不同的是,施艾氏综合征基质中的纤维大小范围很大(19.9至52.0纳米)。此外,纤维直径的分布呈双峰状。X射线衍射证实了基质胶原异常粗大这一发现。结果表明,施艾氏综合征中蛋白聚糖含量/分布与基质破坏之间、基质破坏与角膜混浊之间存在联系。