Figure 9.

Graphic model describing the functional role of Prx1 and Prx1-expressing cells in fracture repair. Following fracture, a population of Prx1+ periosteal and endosteal pericytic cells, co-expressing BMP2 and CXCL12, are elicited and contribute to the cartilaginous and mineralizing calluses, but Prx1’s expression decreases with callus maturation. BMP2’s upregulation after facture leads to a decrease of CXCL12 that in turn down-regulates Prx1, allowing cells to commit to callus maturation. In absence or insufficiency of BMP2 (BMP2^cKO), such regulation of CXCL12 and therefore of Prx1 is lost, leading to abnormal angiogenesis and impaired fracture healing.