Abstract:
STUDY DESIGN:To inhibit β-catenin specifically signaling in chondrocytes Col2-ICAT transgenic mice were generated. Anomalies in caudal vertebrae were detected during embryonic and postnatal stages of Col2-ICAT transgenic mice. OBJECTIVE:To determine the role of canonical β-catenin signaling in caudal vertebral development. SUMMARY OF BACKGROUND DATA:β-catenin signaling plays a critical role in skeletal development. Col2-ICAT transgenic mice were generated to selectively block β-catenin signaling by overexpression of the ICAT gene in chondrocytes. METHODS:Tails of E16.5 transgenic embryos and adult Col2-ICAT transgenic mice and their wild-type littermates were collected and analyzed. Skeletal preparation, 3-dimensional micro-computed tomographic and histological analyses were performed to evaluate changes in the structure of caudal vertebrae. Bromodeoxyuridine labeling was performed to evaluate changes in chondrocyte proliferation in caudal vertebrae. RESULTS:Skeletal preparation and 3-dimensional micro-computed tomographic analyses revealed bone deformation and angulated deformities in tail tissue in Col2-ICAT transgenic mice. Histological studies revealed abnormal bone development and dysplastic caudal vertebrae in Col2-ICAT transgenic mice. Inhibition of β-catenin signaling in cartilage resulted in vertebral dysplasia leading to aberrant resegmenting process. Thus, 2 poorly developed sclerotomes failed to fuse to form a complete vertebrae. BrdU labeling revealed a decreased chondrocyte proliferation in both cartilageous templates of transgenic embryos and the growth plate of adult Col2-ICAT transgenic mice. CONCLUSION:Wnt/β-catenin signaling plays an important role in vertebral development. Inhibition of β-catenin signaling in chondrocytes results in caudal vertebra deformity in mice, which may occur as early as in the stage of sclerotome formation. LEVEL OF EVIDENCE:N/A.
journal_name
Spine (Phila Pa 1976)journal_title
Spineauthors
Shu B,Li TF,Li XF,Tang DZ,Zhang Y,Shi Q,Wang YJ,Chen Ddoi
10.1097/01.brs.0000435024.57940.8dsubject
Has Abstractpub_date
2013-11-15 00:00:00pages
2079-84issue
24eissn
0362-2436issn
1528-1159journal_volume
38pub_type
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