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The osteoinductive properties of prostaglandin E 2  (PGE 2 ) and its signaling pathways have led to suggestions that it may serve as a potential therapeutic strategy for bone loss. However, the prominence of PGE 2  as an inducer of bone formation is attributed primarily to findings from studies using rodent models. In the current study, we investigated the effects of PGE 2  on human bone marrow stromal cell (hBMSC) lineage commitment and determined its mode of action. We demonstrated that PGE 2  treatment of hBMSCs significantly altered the expression profile of several genes associated with osteoblast differentiation ( RUNX2  and  ALP ) and maturation ( BGLAP  and  MGP ). This was attributed to the activation of specific PGE 2  receptors, and was associated with increases in cAMP production and sustained AKT phosphorylation. Pharmacological inhibition of exchange protein directly activated by cAMP (Epac), but not protein kinase A (PKA), recovered the mineralization functions of hBMSC-derived osteoblasts treated with PGE 2  and restored AKT phosphorylation, along with the expression levels of  RUNX2 ,  ALP ,  BGLAP  and  MGP . Our findings therefore provide insights into how PGE 2  influences hBMSC-mediated matrix mineralization, and should be taken into account when evaluating the role of PGE 2  in human bone metabolism.

Prostaglandin E2 inhibits matrix mineralization by human bone marrow stromal cell-derived osteoblasts via Epac-dependent cAMP signaling