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Chondrocyte-specific ablation of Osterix leads to impaired endochondral ossification.

Abstract：

:Osterix (Osx) is an essential transcription factor required for osteoblast differentiation during both intramembranous and endochondral ossification. Endochondral ossification, a process in which bone formation initiates from a cartilage intermediate, is crucial for skeletal development and growth. Osx is expressed in differentiating chondrocytes as well as osteoblasts during mouse development, but its role in chondrocytes has not been well studied. Here, the in vivo function of Osx in chondrocytes was examined in a chondrocyte-specific Osx conditional knockout model using Col2a1-Cre. Chondrocyte-specific Osx deficiency resulted in a weak and bent skeleton which was evident in newborn by radiographic analysis and skeletal preparation. To further understand the skeletal deformity of the chondrocyte-specific Osx conditional knockout, histological analysis was performed on developing long bones during embryogenesis. Hypertrophic chondrocytes were expanded, the formation of bone trabeculae and marrow cavities was remarkably delayed, and subsequent skeletal growth was reduced. The expression of several chondrocyte differentiation markers was reduced, indicating the impairment of chondrocyte differentiation and endochondral ossification in the chondrocyte-specific Osx conditional knockout. Taken together, Osx regulates chondrocyte differentiation and bone growth in growth plate chondrocytes, suggesting an autonomous function of Osx in chondrocytes during endochondral ossification.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Oh JH,Park SY,de Crombrugghe B,Kim JE

doi

10.1016/j.bbrc.2012.01.064

subject

Has Abstract

pub_date

2012-02-24 00:00:00

pages

634-40

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(12)00098-8

journal_volume

418

pub_type

杂志文章

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