The glycosaminoglycans of the human artery and their changes in atherosclerosis.

The glycosaminoglycans of the human artery and their changes in atherosclerosis.
复制标题

人体动脉的糖胺聚糖及其在动脉粥样硬化中的变化。

DOI:
--
复制
发表时间:
1976
影响因子:
15.9
通讯作者:
K. Schmid
K. Schmid
中科院分区:
医学1区
文献类型:
--
作者:
R. Stevens;M. Colombo;J. J. Gonzales;W. Hollander;K. Schmid

文献摘要

被引文献

相似文献

最近引进的双向电泳技术,允许直接测量这些大分子中的每一个的糖胺聚糖(GAGs)的水平的变化,在动脉粥样硬化的人动脉内膜和中膜测定。为了鉴定动脉GAG,通过DEAE-Sephadex A-25柱上的色谱法将它们分级,并且得到三个级分,通过这种电泳方法分析了透明质酸[HA]、硫酸乙酰肝素[HS]和部分分离的硫酸软骨素B [CS B]和C [CSC]的电泳迁移率,分析了它们通过高度特异性水解酶的稳定性(水蛭透明质酸酶、肝素酶和软骨素酶ABC和AC)和它们的艾杜糖醛酸含量。从这些研究中,我们得出结论,正常和动脉粥样硬化的人类动脉含有CSB,CSC,HA和HS。此外,我们证明,CSB是一个混合物组成的约40%CSA和60%CSB和CSC似乎是一种聚合物,基本上由葡萄糖醛酸和N-乙酰半乳糖胺-6-硫酸。经典CSA以及软骨素(CH)不存在可检测的量。在相对正常的内膜中,CSB、CSC、HA和HS的GAG平均浓度分别为4.7、20.9、1.3和5.1 mg/g干燥、脱脂、脱钙组织。随着动脉粥样硬化的进展,总GAG含量显著降低(从32 mg降至18 mg),与CSC和HS水平降低相关,但HA浓度无变化。然而,特别令人感兴趣的是公务员制度委员会的水平有所提高。在总GAG含量平均约为20 mg的培养基中,除CSC外,未观察到这些GAG水平随疾病进展而发生显著变化。这些发现可能是重要的,在解释增加脂蛋白和胶原蛋白沉积在患病的主动脉。
The changes in levels of glycosaminoglycans (GAGs) of the intima and media of the human artery in atherosclerosis were determined by a recently introduced two-dimensional electrophoresis technique that permits direct measurments of each of these macromolecules. To identify the arterial GAGs, they were fractionated by chromatography on a DEAE-Sephadex A-25 column, and the resulting three fractions (hyaluronic acid [HA], heparan sulfate [HS], and the partially separated chondroitin sulfates B [CSB] and C [CSC]) were analyzed for their electrophoretic mobilities by this electrophoretic method, for their digestability by highly specific hydrolases (leech hyaluronidase, heparinase, and chondroitinases ABC and AC) and for their iduronic acid content. From these studies we concluded that normal and atherosclerotic human aortas contain CSB, CSC, HA, and HS. Further, we demonstrated that CSB is a hybrid consisting of approximately 40% CSA and 60% CSB and that CSC appears to be a polymer consisting essentially of glucuronic acid and N-acetylgalactosamine-6-sulfate. Classical CSA as well as chondroitin (CH) were not present in detectable amounts. In the relatively normal intima, the mean concentrations of the GAGs were found to be 4.7, 20.9, 1.3, and 5.1 mg/g of dry, defatted, decalcified tissue for CSB, CSC, HA, and HS, respectively. With the progression of atherosclerosis, there was a pronounced decrease in the total GAG content (from 32 to 18 mg) associated with a decrease in the CSC and HS levels but without a change in the HA concentrations. Of particular interest, however, was the increase in the CSB level. In the media whose total GAG content averaged approximately 20 mg, no significant changes in these GAG levels were noted with the progression of the disease except for that of CSC. These findings may be important in explaining the increased lipoprotein and collagen deposition in the diseased aorta.