INDEPENDENT EXPRESSION OF FIBRIL-FORMING COLLAGEN-I, COLLAGEN-II, AND COLLAGEN-III IN CHONDROCYTES OF HUMAN OSTEOARTHRITIC CARTILAGE

INDEPENDENT EXPRESSION OF FIBRIL-FORMING COLLAGEN-I, COLLAGEN-II, AND COLLAGEN-III IN CHONDROCYTES OF HUMAN OSTEOARTHRITIC CARTILAGE
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DOI:
10.1172/jci116303
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发表时间:
1993-03-01
影响因子:
15.9
通讯作者:
VONDERMARK, K
VONDERMARK, K
中科院分区:
医学1区
文献类型:
--
作者:
AIGNER, T;BERTLING, W;VONDERMARK, K

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通过原位杂交研究正常和骨关节炎患者关节软骨纤维I型、II型和III型胶原的表达模式,以评估关节软骨细胞与疾病相关的表型变化。在20个样本中的11个样本中,骨关节炎软骨表面和中上区的软骨细胞亚群显示出显著水平的细胞质α 1 (III) mRNA,而在中上和中下区发现了α 1 (II) mRNA的强信号,部分与α 1 (III) mRNA表达细胞区重叠。II型和III型胶原表达的程度取决于软骨细胞周围细胞外基质的完整性以及关节软骨内的位置。骨关节炎原关节软骨中未检测到alpha1 (1) mRNA。然而,alpha1(I)探针确实显示了潘瘤样组织、骨赘和骨细胞中的信号。在正常关节软骨中,没有检测到细胞质中α 1 (I)、α 2 (I)或α 1 (III) mRNA的水平。使用特异性单克隆抗体和多克隆抗体,我们发现在骨关节炎软骨的浅表区沉积了III型胶原,但几乎没有任何I型胶原,这与原位杂交结果一致。这些结果表明,在病变软骨条件下,软骨细胞的特定亚群中存在表型改变,表达和合成III型胶原蛋白独立于I型胶原蛋白,但部分与II型胶原蛋白同时表达和合成。
Normal and osteoarthritic human articular cartilage was investigated by in situ hybridization for expression patterns of the fibrillar collagens type I, II, and III to evaluate phenotypic changes of articular chondrocytes related to the disease. In 11 out of 20 samples, a defined subset of chondrocytes in the superficial and upper middle zone of osteoarthritic cartilage showed significant levels of cytoplasmic alpha1 (III) mRNA, whereas strong signals of alpha1 (II) mRNA were found in the upper and lower middle zone, partially overlapping with the zone of alpha1 (III) mRNA-expressing cells. The extent of type II and III collagen expression depended on the integrity of the extracellular matrix surrounding the chondrocytes, and the location within the articular cartilage. No alpha1 (1) mRNA was detectable in osteoarthritic original articular cartilage. The alpha1(I) probe did, however, reveal signals in pannuslike tissue, osteophytes, and bone cells. In normal articular cartilage, no detectable levels of cytoplasmic mRNA for alpha1 (I), alpha2 (I), or alpha1 (III) were seen. Using specific mono- and polyclonal antibodies, we found deposition of type III collagen but hardly any of type I collagen in the superficial zone of osteoarthritic cartilage that is consistent with the in situ hybridization results.These results indicate a phenotypic alteration in a defined subset of chondrocytes in conditions of diseased cartilage, expressing and synthesizing collagen type III independently from type I collagen, but in part simultaneously with type II collagen.