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首页> 外文期刊>BMC Musculoskeletal Disorders >Expression of minor cartilage collagens and small leucine rich proteoglycans may be relatively reduced in osteoarthritic cartilage
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Expression of minor cartilage collagens and small leucine rich proteoglycans may be relatively reduced in osteoarthritic cartilage

机译：骨关节炎软骨中相对较小的软骨胶原蛋白和富含亮氨酸的小蛋白聚糖的表达可能相对减少

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In osteoarthritis (OA), cartilage matrix is lost despite vigorous chondrocyte anabolism. In this study, we attempted to determine whether altered matrix synthesis is involved in this paradox in disease progression through gene expression analysis and ultrastructural analysis of collagen fibrils within the cartilage matrix. Cartilage tissues were obtained from 29 end-stage OA knees and 11 control knees. First, cDNA microarray analysis was performed and the expression of 9 genes involved in collagen fibrillogenesis was compared between OA and control cartilages. Then their expression was investigated in further detail by a quantitative polymerase chain reaction (qPCR) analysis combined with laser capture microdissection. Finally, collagen fibril formation was compared between OA and control cartilage by transmission electron microscopy. The result of the microarray analysis suggested that the expression of type IX and type XI collagens and fibrillogenesis-related small leucine-rich proteoglycans (SLRPs) may be reduced in OA cartilage relative to the type II collagen expression. The qPCR analysis confirmed these results and further indicated that the relative reduction in the minor collagen and SLRP expression may be more obvious in degenerated areas of OA cartilage. An ultrastructural analysis suggested that thicker collagen fibrils may be formed by OA chondrocytes possibly through reduction in the minor collagen and SLRP expression. This may be the first study to report the possibility of altered collagen fibrillogenesis in OA cartilage. Disturbance in collagen fibril formation may be a previously unidentified mechanism underlying the loss of cartilage matrix in OA.
机译：在骨关节炎（OA）中，尽管软骨细胞合成代谢旺盛，软骨基质仍会丢失。在这项研究中，我们试图通过基因表达分析和软骨基质内胶原纤维的超微结构分析来确定改变的基质合成是否参与疾病发展的这一悖论。从29个末期OA膝和11个对照膝获得软骨组织。首先，进行cDNA微阵列分析，并比较OA和对照软骨中9种参与胶原纤维形成的基因的表达。然后，通过定量聚合酶链反应（qPCR）分析与激光捕获显微切割相结合，进一步研究了它们的表达。最后，通过透射电子显微镜比较了OA和对照软骨之间的胶原原纤维形成。微阵列分析的结果表明，相对于II型胶原蛋白表达，IX软骨中IX和XI型胶原蛋白的表达以及与原纤维形成相关的富含亮氨酸的小蛋白聚糖（SLRPs）可能减少。 qPCR分析证实了这些结果，并进一步表明，在OA软骨退化区域，次要胶原蛋白和SLRP表达的相对减少可能更为明显。超微结构分析表明，OA软骨细胞可能形成较厚的胶原纤维，可能是通过减少次要胶原蛋白和SLRP表达而形成的。这可能是第一个报道OA软骨胶原纤维化发生改变的可能性的研究。胶原蛋白原纤维形成的紊乱可能是OA中软骨基质丧失的潜在机制。

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