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Alterations in the chondroitin sulfate chain in human osteoarthritic cartilage of the knee

机译：膝关节骨性关节炎软骨中硫酸软骨素链的改变

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Objective: To determine whether the structure of chondroitin sulfate (CS) in cartilage is reflected by the degree of cartilage degeneration in patients with osteoarthritis (OA) of the knee and to determine how CS biosynthesis affects cartilage degeneration. Design: Two osteoarthritic cartilage samples were obtained from medial femoral condyle (MFC) and lateral femoral condyle (LFC) of 24 knees with end-stage OA. The samples were assigned to two groups as follows: lesion and remote cartilage were adjacent to and remote from the osteoarthritic cartilage, respectively. Histological grade was determined according to the Mankin score. The CS concentration and chain length were determined using high-performance liquid chromatography (HPLC) and gel filtration chromatography, respectively. Expression of the gene encoding CS glycosyltransferase was evaluated using a real-time quantitative polymerase chain reaction (qPCR) assay. These results were compared between lesion and remote cartilage. Results: The Mankin score indicated that lesion cartilage was more degraded compared with remote cartilage. Although the CS levels varied among individuals, the mean CS concentration and chain length were significantly lower and shorter in lesion cartilage than in remote cartilage, respectively (concentration: 12.04 vs 14.84μg/mg wet weight, P=0.021; chain length: 5.36 vs 6.19kDa, P=0.026). Three genes encoding CS glycosyltransferases (CHPF, CSGALNACT1, CSGALNACT2) were expressed at lower levels in lesion cartilage. Conclusions: In the osteoarthritic knee, the CS concentration and chain length were reduced closer to the more degraded cartilage with decreasing CS glycosyltransferase gene expression. Inhibition of CS glycosyltransferase gene expression may reduce CS chain length, which may contribute to OA progression.
机译：目的：确定膝关节骨关节炎（OA）患者的软骨变性程度是否可以反映软骨中硫酸软骨素（CS）的结构，并确定CS生物合成如何影响软骨变性。设计：从24膝终末OA的股骨内侧fe（MFC）和外侧股骨con（LFC）获得两个骨关节炎软骨样品。将样品分为两组：病变和远端软骨分别邻近和远离骨关节炎软骨。组织学等级根据Mankin评分确定。 CS浓度和链长分别使用高效液相色谱（HPLC）和凝胶过滤色谱法测定。使用实时定量聚合酶链反应（qPCR）分析评估编码CS糖基转移酶的基因的表达。比较了病变和远端软骨的这些结果。结果：Mankin评分表明，与远端软骨相比，病变软骨的降解程度更高。尽管个体之间的CS水平有所不同，但病变软骨的平均CS浓度和链长分别比远侧软骨低得多和短（浓度：湿重12.04vs.14.84μg/ mg，P = 0.021;链长：5.36 vs 6.19kDa，P ＝ 0.026）。编码CS糖基转移酶的三个基因（CHPF，CSGALNACT1，CSGALNACT2）在病变软骨中的表达水平较低。结论：随着CS糖基转移酶基因表达的降低，在骨关节炎膝关节中，CS浓度和链长降低得更接近于更退化的软骨。 CS糖基转移酶基因表达的抑制可能会减少CS链的长度，这可能有助于OA进展。

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