The aim of this study was to ascertain whether, like many cell types in cartilaginous tissues if type XI collagen was a pericellular component of annulus fibrosus (AF) cells and chondrocytes. Fine fibrillar networks were visualised which were perlecan, HS (MAb 10E4) and type XI collagen positive. Heparitinase-III pre-digestion abolished the type XI collagen and 10E4 localisation in these fibrillar assemblies demonstrating a putative HS mediated interaction which localised the type XI collagen. Type XI collagen was confirmed to be present in the Heparitinase III treated AF monolayer media samples by immunoblotting. Heparitinase-III generated ΔHS stub epitopes throughout these fibrillar networks strongly visualised by MAb 3-G-10. Monolayers of murine hip articular chondrocytes from C57BL/6 and Hspg2 exon 3 null mice also displayed pericellular perlecan localisations, however type XI collagen was only evident in the Wild type mice. Perlecan was also immunolocalised in control and murine knee articular cartilage from the two mouse genotypes subjected to a medial meniscal destabilisation procedure which induces OA. This resulted in a severe depletion of perlecan levels particularly in the perlecan exon 3 null mice and was consistent with OA representing a disease of the pericellular matrix. A model was prepared to explain these observations between the NPP type XI collagen domain and HS chains of perlecan domain-I in the pericellular matrix of AF cells which likely contributed to cellular communication, tissue stabilization and the regulation of extracellular matrix homeostasis.

中文翻译：

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XI型胶原蛋白-perlecan-HS相互作用可稳定纤维环细胞和软骨细胞的细胞周围基质，从而提供基质稳定和体内平衡。

这项研究的目的是确定是否像软骨组织中的许多细胞类型一样，XI型胶原是否是纤维环（AF）细胞和软骨细胞的细胞周围成分。可视化的细纤维网络为perlecan，HS（MAb 10E4）和XI型胶原阳性。肝素酶-III的预消化消除了这些原纤维组件中的XI型胶原蛋白和10E4的定位，这证明了假定的HS介导的相互作用将XI型胶原蛋白定位了。通过免疫印迹证实了在肝素酶III处理的AF单层培养基样品中存在XI型胶原。肝素酶III在MAb 3-G-10强烈显现的整个这些原纤维网络中生成了ΔHS残基表位。C57BL / 6和Hspg2的小鼠髋关节软骨细胞的单层外显子3无效的小鼠也表现出细胞周围的Perlecan定位，但是XI型胶原仅在野生型小鼠中明显。Perlecan也被免疫定位于来自两种小鼠基因型的对照和鼠膝关节软骨中，这两种基因型经历了诱导OA的内侧半月板失稳过程。这导致全白蛋白水平的严重消耗，尤其是在全白蛋白外显子3无效小鼠中，并且与代表细胞周基质疾病的OA一致。制备模型以解释AF细胞周基质中NPP型XI胶原结构域和Perlecan域-I HS链之间的这些观察结果，这可能有助于细胞通讯，组织稳定和细胞外基质稳态的调节。