Localization of the expression of type I, II and III collagen genes in human normal and hypochondrogenesis cartilage canals

Localization of the expression of type I, II and III collagen genes in human normal and hypochondrogenesis cartilage canals
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人类正常和软骨形成软骨管中 I、II 和 III 型胶原蛋白基因表达的定位

DOI:
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发表时间:
1994
期刊:
The Histochemical Journal
影响因子:
--
通讯作者:
D. Herbage
D. Herbage
中科院分区:
--
文献类型:
--
作者:
D. Guellec;F. Mallein;I. Treilleux;J. Bonaventure;P. Peysson;D. Herbage

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本研究应用电泳分析、免疫组织化学和原位杂交技术检测了人正常和软骨发育不良软骨管中I、II和III型胶原基因的表达,结果表明,在正常软骨中,I、III型胶原存在于软骨膜、软骨管血管周围结缔组织和致密纤维组织中。然而,I型和III型前胶原mRNA仅在软骨膜和根管的成纤维细胞中检测到,但在多态性细胞中未检测到。II型胶原蛋白存在于软骨基质和致密的纤维组织中,与在软骨细胞和多态性细胞中检测到的II型前胶原mRNA的定位完全一致。这些数据表明,不存在表达I型、II型和III型胶原基因的移行细胞,并且多态性细胞起源于软骨细胞。在软骨发育不全的情况下,II型胶原蛋白的丰度低于正常软骨,而相应的mRNA水平是相等的。这表明该蛋白质的转录后调节参与了II型胶原蛋白产生的减少。I型胶原蛋白,出乎意料地检测到在软骨基质中,由软骨细胞和多态性细胞合成,这表明II型胶原蛋白的I型替代。因此,在这种病理情况下观察到的管肥大可能是由于有缺陷的软骨基质引起的软骨管生长调节的改变。
SummaryThe 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.
DOI: 10.1016/s0021-9258(17)36881-3
发表时间: 1994-05
期刊: The Journal of biological chemistry
影响因子: --
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DOI: --
发表时间: 1986
影响因子: 9.8
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发表时间: 1992-05
影响因子: 11.1
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DOI: 10.1016/s0021-9258(18)41703-6
发表时间: 1992-11
期刊: The Journal of biological chemistry
影响因子: --
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通讯作者: R. Bogaert;G. Tiller;MaryAnn Weis;H. Gruber;D. L. Rimoin;Daniel H. Cohn;D. Eyre
DOI: --
发表时间: 1985
期刊: The Journal of biological chemistry
影响因子: --
作者:
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通讯作者: Ramirez,F