Wnt gene expression in the post-natal growth plate: Regulation with chondrocyte differentiation

被引:100
作者
Andrade, Anenisla C. [1 ]
Nilsson, Ola [1 ]
Barnes, Kevin M. [1 ]
Baron, Jeffrey [1 ]
机构
[1] NICHHD, Dev Endocrinol Branch, NIH, Bethesda, MD 20892 USA
关键词
Wnt; growth plate; chondrocyte; cartilage;
D O I
10.1016/j.bone.2007.01.005
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Longitudinal growth of long bones occurs at the growth plate by endochondral ossification. In the embryonic mouse, this process is regulated by Writ signaling. Little is known about which members of the Writ family of secreted signaling proteins might be involved in the regulation of the postnatal growth plate. We used microdissection and real-time PCR to study mRNA expression of Writ genes in the mouse growth plate. Of the 19 known members of the Writ family, only six were expressed in postnatal growth plate. Of these, Writs -2b, -4, and -10b signal through the canonical beta-catenin pathway and Writs -5a, -5b, and -11 signal through the noncanonical calcium pathway. The spatial expression for these six Writs was remarkably similar, showing low mRNA expression in the testing zone, increasing expression as the chondrocytes differentiated into the proliferative and prehypertrophic state and then (except Wnt-2b) decreasing expression as the chondrocytes underwent hypertrophic differentiation. This overall pattern is broadly consistent with previous studies of embryonic mouse growth cartilage Suggesting that Writ signaling modulates chondrocyte proliferation and hypertrophic differentiation. We also found that mRNA expression of these Writ genes persisted at similar levels at 4 weeks, when longitudinal bone growth is waning. In conclusion, we have identified for the first time the specific Writ genes that are expressed in the postnatal mammalian growth plate. The six identified Writ genes showed a similar pattern of expression during chondrocyte differentiation, suggesting overlapping or interacting roles in postnatal endochondral bone formation. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:1361 / 1369
页数:9
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