Osteoblast-derived PTHrP is a physiological regulator of bone formation
J. Clin. Invest. T. John Martin, et al. 115:2322 doi:10.1172/JCI26239 [Go to this article.]

Figure 1
Paracrine actions of PTHrP in bone. Osteoblast progenitors in bone and bone marrow produce PTHrP that acts through PTHR1 on committed preosteoblasts to enhance their differentiation to mature, matrix-producing osteoblasts. The second major effect related to stimulation of bone formation is the action of PTHrP on both mature osteoblasts and osteocytes to reduce apoptosis. For PTHrP to generate an anabolic response, it needs to be presented to its targets transiently (16–18). The effect of PTHrP on the bone resorption pathway is depicted, with PTHrP acting through PTHR1 on cells of the osteoblast lineage, which respond with increased production of RANKL. This requires more prolonged stimulation by PTHrP (17, 18), and the location of these responsive cells is such that RANKL can interact with its receptor, RANK, on hemopoietic precursors to promote increased osteoclast formation and activity. In each of its local actions the potential exists for other biological activities of PTHrP to be exerted on its target cells.