DOI: 10.1101/470005Nov 14, 2018Paper

Chondrocyte-specific RUNX2 Overexpression Causes Chondrodysplasia During Development, but is Not Sufficient to Induce OA-like Articular Cartilage Degeneration in Adult Mice Without Injury

BioRxiv : the Preprint Server for Biology
Sarah E CathelineJennifer H Jonason


RUNX2 is a transcription factor critical for chondrocyte maturation and normal endochondral bone formation. It promotes the expression of factors catabolic to the cartilage extracellular matrix and is shown to be upregulated in human osteoarthritic cartilage and in murine articular cartilage following joint injury. To date, in vivo studies of RUNX2 overexpression in cartilage have been limited to forced expression in osteochondroprogenitor cells preventing investigation into the effects of chondrocyte-specific RUNX2 overexpression during development or in postnatal articular cartilage. Here, we used the Rosa26Runx2 allele in combination with the inducible Col2a1CreERT2 transgene or the inducible AcanCreERT2 knock-in allele to achieve chondrocyte-specific RUNX2 overexpression (OE) during embryonic development or in the postnatal articular cartilage of adult mice, respectively. RUNX2 OE was induced at E13.5 for all developmental studies and resulted in a phenotype resembling chondrodysplasia at E18.5. Histology and in situ hybridization analyses suggest an early onset of chondrocyte hypertrophy and accelerated terminal maturation in the limbs of the RUNX2 OE embryos compared to control embryos. Additionally, RUNX2 OE resulted in ...Continue Reading

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