Journal
JOURNAL OF CELL SCIENCE
Volume 121, Issue 9, Pages 1455-1465Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.020362
Keywords
chondrocyte; endochondral bone formation; inhibitor of beta-catenin and TCF (ICAT); vascular endothelial growth factor (VEGF); beta-catenin
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Funding
- NIAMS NIH HHS [R01 AR053717, R01 AR051189-04, K02 AR052411-01A2, R01 AR051189, AR 054465, R01 AR051189-02, K02 AR052411, K02 AR052411-02, R01 AR054465-02, R01 AR054465, R01 AR038945, R01 AR051189-03, R01 AR054465-01, AR 038945, AR 053717] Funding Source: Medline
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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.
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