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首页> 外文期刊>Osteoarthritis and cartilage >Contacts with fibrils containing collagen I, but not collagens II, IX, and XI, can destabilize the cartilage phenotype of chondrocytes.
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Contacts with fibrils containing collagen I, but not collagens II, IX, and XI, can destabilize the cartilage phenotype of chondrocytes.

机译：与含有胶原蛋白I但不含胶原蛋白II，IX和XI的原纤维接触会破坏软骨细胞的软骨表型。

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OBJECTIVE: Cell-matrix interactions are important regulators of cellular functions, including matrix synthesis, proliferation and differentiation. This is well exemplified by the characteristically labile phenotype of chondrocytes that is lost in monolayer culture but is stabilized in suspension under appropriate conditions. We were interested in the role of collagen suprastructures in maintaining or destabilizing the cartilage phenotype of chondrocytes. DESIGN: Primary sternal chondrocytes from 17-day-old chick embryos were cultured in gels of fibrils reconstituted from soluble collagen I from various sources. The culture media either contained or lacked FBS. Cells were cultured for up to 28 days and the evolution of the phenotype of the cells was assessed by their collagen expression (collagens II and X for differentiated chondrocytes and hypertrophic chodrocytes, repectively; collagen I for phenotypically modulated cells), or by their secretion of alkaline phosphatase (hypertrophic cartilage phenotype). RESULTS: The cells often retained their differentiated phenotype only if cultured with serum. Under serum-free conditions, cartilage characteristics were lost. The cells acquired a fibroblast-like shape and, later, synthesized collagen I instead of cartilage collagens. Shape changes were influenced by beta1-integrin-activity, whereas other matrix receptors were important for alterations of collagen patterns. Heterotypic fibrils reconstituted from collagens II, IX, and XI did not provoke this phenotypic instability. CONCLUSIONS: Chondrocytes sensitively recognize the suprastructures of collagen fibrils in their environment. Cellular interactions with fibrils with appropriate molecular organizations, such as that in cartilage fibrils, result in the maintenance of the differentiated cartilage phenotype. However, other suprastructures, e.g. in reconstituted fibrils mainly containing collagen I, lead to cell-matrix interactions incompatible with the cartilage phenotype. The maintenance of the differentiated traits of chondrocytes is pivotal for the normal function of, e.g., articular cartilage. If pathologically altered matrix suprastructures lead to a dysregulation of collagen production also in vivo compromised cartilage functions inevitably will be propagated further.
机译：目的：细胞-基质相互作用是细胞功能的重要调节剂，包括基质合成，增殖和分化。软骨细胞的特征不稳定表型很好地说明了这一点，该表型在单层培养中丢失但在适当条件下在悬浮液中稳定。我们对胶原超结构在维持或破坏软骨细胞软骨表型中的作用感兴趣。设计：将来自17天大的雏鸡胚胎的原始胸骨软骨细胞培养在原纤维的凝胶中，原纤维由多种来源的可溶性胶原蛋白I重构而成。培养基含有或缺乏FBS。将细胞培养长达28天，并通过胶原蛋白的表达（分别针对分化的软骨细胞和肥大性软骨细胞的胶原II和X;针对表型调节的细胞的胶原I）评估细胞表型的演变。碱性磷酸酶（肥大性软骨表型）。结果：仅当与血清一起培养时，细胞通常才保留其分化表型。在无血清条件下，软骨特性丧失。这些细胞获得了成纤维细胞状的形状，后来合成了胶原蛋白I，而不是软骨胶原蛋白。形状变化受β1-整合素活性的影响，而其他基质受体对于改变胶原蛋白的模式很重要。由胶原蛋白II，IX和XI重构的异型原纤维没有引起这种表型不稳定性。结论：软骨细胞在其周围环境中敏感地识别胶原纤维的超结构。与具有适当分子组织的原纤维的细胞相互作用，例如软骨原纤维中的相互作用，导致分化软骨表型的维持。但是，其他上部结构，例如在主要含有胶原蛋白I的重组原纤维中，β-内啡肽导致与软骨表型不相容的细胞-基质相互作用。软骨细胞分化特性的维持对于例如关节软骨的正常功能至关重要。如果病理改变的基质超结构导致胶原蛋白生产失调，那么体内受损的软骨功能也将不可避免地进一步传播。

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