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Expression patterns of chondrocyte genes cloned by differential display in tibial dyschondroplasia
被引:21
|作者:
Jefferies, D
[1
]
Houston, B
[1
]
Lester, D
[1
]
Whitehead, CC
[1
]
Thorp, BH
[1
]
Botman, M
[1
]
Farquharson, C
[1
]
机构:
[1] Roslin Inst, Bone Biol Grp, Div Integrat Biol, Roslin EH25 9PS, Midlothian, Scotland
来源:
关键词:
growth plate chondrocyte;
gene expression;
differential display;
tibial dyschondroplasia;
D O I:
10.1016/S0925-4439(00)00020-X
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Tibial dyschondroplasia (TD) appears to involve a failure of the growth plate chondrocytes within growing long bones to differentiate fully to the hypertrophic stage, resulting in a mass of prehypertrophic chondrocytes which form the avascular TD lesion. Many biochemical and molecular markers of chondrocyte hypertrophy are absent from the lesion, or show reduced expression, but the cause of the disorder remains to be identified. As differentiation to the hypertrophic state is impaired in TD, we hypothesised that chondrocyte genes that are differentially expressed in the growth plate should show altered expression in TD. Using differential display, four genes, B-cadherin, EF2, HT7 and Ex-FABP were cloned from chondrocytes stimulated to differentiate to the hypertrophic stage in vitro, and their differential expression confirmed in vivo. Using semi-quantitative RT-PCR, the expression patterns of these genes were compared in chondrocytes from normal and TD growth plates. Surprisingly, none of these genes showed the pattern of expression that might be expected in TD lesion chondrocytes, and two of them, B-cadherin and Ex-FABP, were upregulated in the lesion. This indicates that the TD phenotype does not merely reflect the absence of hypertrophic marker genes, but may be influenced by more complex developmental mechanisms/defects than previously thought. (C) 2000 Elsevier Science B.V. All rights reserved.
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页码:180 / 188
页数:9
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