Le Guellec D, Mallein-Gerin F, Treilleux I, Bonaventure J, Peysson P, Herbage D
Laboratoire de Cytologie Moléculaire CNRS UPR 412, Institut de Biologie et Chimie des Protéines, Lyon, France.
Histochem J. 1994 Sep;26(9):695-704. doi: 10.1007/BF00158202.
The expression of type I, II and III collagens genes was examined in human normal and hypochondrogenesis cartilage canals employing electrophoretic analysis, immunohistochemistry and in situ hybridization techniques. In normal cartilage, collagens type I and III were present in perichondrium, in the connective tissue surrounding the vessels of cartilage canals and in the dense fibrous tissue. However, types I and III procollagen mRNAs were detected only in fibroblasts of the perichondrium and of the canals, but not in the polymorphic cells. Type II collagen was present in the cartilage matrix and in the dense fibrous tissue, in good accordance with the localization of type II procollagen mRNAs detected in the chondrocytes and in the polymorphic cells. These data suggest that there are no transitional cells expressing type I, II and III collagen genes and that polymorphic cells are of chondrocytic origin. In the case of hypochondrogenesis, type II collagen was less abundant than in normal cartilage, whereas the corresponding mRNA level was equivalent. That suggests that a postranscriptional regulation of this protein is involved in the decrease of type II collagen production. Type I collagen, unexpectedly detected in the cartilage matrix, was synthesized by chondrocytes and polymorphic cells, suggesting a replacement of type II by type I collagen. The canal hypertrophy observed in this pathological case could thus be due to a modification in the regulation of the growth of cartilage canals caused by a defective cartilage matrix.
采用电泳分析、免疫组织化学和原位杂交技术，检测了人正常软骨和软骨发育不全软骨管中I型、II型和III型胶原基因的表达。在正常软骨中，I型和III型胶原存在于软骨膜、软骨管血管周围的结缔组织以及致密纤维组织中。然而，仅在软骨膜和成管细胞的成纤维细胞中检测到I型和III型前胶原mRNA，而在多形细胞中未检测到。II型胶原存在于软骨基质和致密纤维组织中，与在软骨细胞和多形细胞中检测到的II型前胶原mRNA的定位一致。这些数据表明，不存在表达I型、II型和III型胶原基因的过渡细胞，多形细胞起源于软骨细胞。在软骨发育不全的情况下，II型胶原比正常软骨中含量少，而相应的mRNA水平相当。这表明该蛋白的转录后调控参与了II型胶原产生的减少。意外地在软骨基质中检测到I型胶原，它由软骨细胞和多形细胞合成，提示I型胶原取代了II型胶原。因此，在这种病理情况下观察到的管肥大可能是由于软骨基质缺陷导致软骨管生长调节改变所致。
