MODULATION AND REEXPRESSION OF THE CHONDROCYTE PHENOTYPE - MEDIATION BY CELL-SHAPE AND MICROFILAMENT MODIFICATION

MODULATION AND REEXPRESSION OF THE CHONDROCYTE PHENOTYPE - MEDIATION BY CELL-SHAPE AND MICROFILAMENT MODIFICATION
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DOI:
10.1159/000157093
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发表时间:
1988-01-01
期刊:
PATHOLOGY AND IMMUNOPATHOLOGY RESEARCH
影响因子:
--
通讯作者:
BENYA, PD
BENYA, PD
中科院分区:
其他
文献类型:
--
作者:
BENYA, PD

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评价软骨细胞以鉴定导致软骨营养不良发病机制的遗传缺陷将需要增加最初可用的少量细胞同时维持或重新获得其分化表型的方法。要实现这些目标,就需要更深入地了解影响文化中分化状态表达的因素和调节机制。由于一些缺陷可能是在调节途径,而不是在基质分子的结构,在正常软骨细胞的识别和表征,这样的路径的方式,应允许随后测试其完整性软骨营养不良软骨软骨细胞。作为一种高度特化的细胞,软骨细胞产生并维持软骨细胞外基质,并且在某些情况下为血管侵入和成骨准备环境。除了其主要的生物合成产物的软骨特异性胶原和蛋白多糖,复杂的,分化的表型包括其他基质分子和细胞内分子的结构和调节功能。当同时测定表型的多个元素时。它们似乎是协调调节的[1-3]。因此,我们已经利用遗传上不同的胶原类型的表达的变化来监测分化的软骨细胞表型的调节[3-5]和再表达[1,6]。
Evaluation of chondrocytes to identify ge netic defects responsible for the pathogenesis of the chondrodystrophies will require meth ods for increasing the small number of cells initially available while maintaining or re gaining their differentiated phenotype. At tainment of these goals will require a greater understanding of factors and regulatory mechanisms that influence the expression of the differentiated state in culture. Since some defects may be in regulatory pathways and not in the structure of matrix molecules, iden tification and characterization of such path ways in normal chondrocytes should allow subsequent testing of their integrity in chon drocytes from chondrodystrophic cartilage. As a highly specialized cell the chondro cyte produces and maintains the cartilage extracellular matrix, and in some circum stances prepares an environment for vascu lar invasion and osteogenesis. In addition to its principal biosynthetic products of carti lage-specific collagens and proteoglycans, the complex, differentiated phenotype con sists of other matrix molecules and intracel lular molecules of both structural and regula tory function. When multiple elements of the phenotype have been assayed simulta neously. they appear to be coordinately regu lated [1-3]. Consequently, we have utilized changes in the expression of the genetically distinct collagen types to monitor the modu lation [3-5] and reexpression [1, 6] of the differentiated chondrocyte phenotype.