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

被引:211
作者
AIGNER, T
BERTLING, W
STOSS, H
WESELOH, G
VONDERMARK, K
机构
[1] UNIV ERLANGEN NURNBERG,MED CLIN 3,CLIN RES GRP RHEUMATOL,MAX PLANCK SOC,W-8520 ERLANGEN,GERMANY
[2] UNIV ERLANGEN NURNBERG,MED CLIN 3,DEPT ORTHOPAED,W-8520 ERLANGEN,GERMANY
[3] UNIV ERLANGEN NURNBERG,MED CLIN 3,DEPT PATHOL,W-8520 ERLANGEN,GERMANY
关键词
CHONDROCYTES; INSITU HYBRIDIZATION; COLLAGEN MESSENGER RNA; ARTICULAR CARTILAGE; IMMUNOHISTOCHEMISTRY;
D O I
10.1172/JCI116303
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 [基础医学];
摘要
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.
引用
收藏
页码:829 / 837
页数:9
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