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. Author manuscript; available in PMC: 2017 Apr 1.
Published in final edited form as: Bone. 2016 Feb 3;85:123–130. doi: 10.1016/j.bone.2016.01.023

Fig. 6. Proposed means by which PTH inhibits its own osteogenic/anabolic actions.

Fig. 6

PTH stimulates Rankl and Cox2/PGE2 in osteoblast (OB) lineage cells. Rankl acts on osteoclast (OC) lineage cells to commit them to become osteoclasts and to stimulate more Cox2/PGE2. The combination of Rankl and PGE2 cause cells committed to become osteoclasts to secrete Saa3. In the presence of Saa3, PTH-stimulated cAMP production is abrogated, preventing subsequent PKA activation and β-catenin signaling. When PTH is unable to initiate this negative feedback pathway, either by absence of osteoclasts or Cox2, β-catenin is phosphorylated at Ser552 and Ser675 and can stimulate gene transcription associated with osteoblastic differentiation.