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Antxr1/Tem8 is highly expressed in tumor endothelial cells and is a receptor for anthrax toxin. Mutation of  Antxr1  causes GAPO syndrome, which is characterized by growth retardation, alopecia, pseudo-anodontia, and optic atrophy. However, the mechanism underlying the growth retardation remains to be clarified. Runx2 is essential for osteoblast differentiation and chondrocyte maturation and regulates chondrocyte proliferation through  Ihh  induction. In the search of Runx2 target genes in chondrocytes, we found that  Antxr1  expression is upregulated by Runx2.  Antxr1  was highly expressed in cartilaginous tissues and was directly regulated by Runx2. In skeletal development, the process of endochondral ossification proceeded similarly in wild-type and  Antxr1  –/–  mice. However, the limbs of  Antxr1  –/–  mice were shorter than those of wild-type mice from embryonic day 16.5 due to the reduced chondrocyte proliferation. Chondrocyte-specific  Antxr1  transgenic mice exhibited shortened limbs, although the process of endochondral ossification proceeded as in wild-type mice. BrdU-uptake and apoptosis were both increased in chondrocytes, and the apoptosis-high regions were mineralized. These findings indicated that Antxr1, of which the expression is regulated by Runx2, plays an important role in chondrocyte proliferation and that overexpression of  Antxr1  causes chondrocyte apoptosis accompanied by matrix mineralization.

Antxr1, Which is a Target of Runx2, Regulates Chondrocyte Proliferation and Apoptosis