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J Cell Sci. 2008 May 1;121(Pt 9):1455-65. doi: 10.1242/jcs.020362. Epub 2008 Apr 8.

Inhibition of beta-catenin signaling causes defects in postnatal cartilage development.

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1
Department of Orthopaedics, Center for Musculoskeletal Research, University of Rochester School of Medicine, Rochester, NY 14642, USA.

Abstract

The Wnt/beta-catenin signaling pathway is essential for normal skeletal development because conditional gain or loss of function of beta-catenin in cartilage results in embryonic or early postnatal death. To address the role of beta-catenin in postnatal skeletal growth and development, Col2a1-ICAT transgenic mice were generated. Mice were viable and had normal size at birth, but became progressively runted. Transgene expression was limited to the chondrocytes in the growth plate and articular cartilages and was associated with decreased beta-catenin signaling. Col2a1-ICAT transgenic mice showed reduced chondrocyte proliferation and differentiation, and an increase in chondrocyte apoptosis, leading to decreased widths of the proliferating and hypertrophic zones, delayed formation of the secondary ossification center, and reduced skeletal growth. Isolated primary Col2a1-ICAT transgenic chondrocytes showed reduced expression of chondrocyte genes associated with maturation, and demonstrated that VEGF gene expression requires cooperative interactions between BMP2 and beta-catenin signaling. Altogether the findings confirm a crucial role for Wnt/beta-catenin in postnatal growth.

PMID:
18397998
PMCID:
PMC2636704
DOI:
10.1242/jcs.020362
[Indexed for MEDLINE]
Free PMC Article

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