These authors found that Schnurri-3 (Shn3) plays no cell-intrinsic role in osteoclasts. However, Shn3-deficient animals had decreased serum markers of bone turnover. In addition, selective deletion of Shn3 in the mesenchymal lineage in mice recapitulated the high bone mass phenotype of global Shn3 KO mice, including reduced osteoclastic bone catabolism in vivo. These findings indicate that Shn3 expression in mesenchymal cells directly controls osteoblastic bone formation and indirectly regulates osteoclastic bone resorption.
Wein MN, Jones DC, Shim JH, Aliprantis AO, Sulyanto R, Lazarevic V, et al.