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The Wnt signaling pathway is a robust regulator of skeletal homeostasis. Gain-of-function mutations promote high bone mass, whereas loss of Lrp5 or Lrp6 co-receptors decrease bone mass. Similarly, mutations in antagonists of Wnt signaling influence skeletal integrity, in an inverse relation to Lrp receptor mutations. Loss of the Wnt antagonist Sclerostin ( Sost ) produces the generalized skeletal hyperostotic condition of sclerosteosis, which is characterized by increased bone mass and density due to hyperactive osteoblast function. Here we demonstrate that prostaglandin E 2  (PGE 2 ), a paracrine factor with pleiotropic effects on osteoblasts and osteoclasts, decreases Sclerostin expression in osteoblastic UMR106.01 cells. Decreased  Sost  expression correlates with increased expression of Wnt/TCF target genes  Axin2  and  Tcf3 . We also show that the suppressive effect of PGE 2  is mediated through a cyclic AMP/PKA pathway. Furthermore, selective agonists for the PGE 2  receptor EP2 mimic the effect of PGE 2  upon  Sost , and siRNA reduction in  Ptger2  prevents PGE 2 -induced  Sost  repression. These results indicate a functional relationship between prostaglandins and the Wnt/β-catenin signaling pathway in bone.

Prostaglandin E2 Signals Through PTGER2 to Regulate Sclerostin Expression