| First Author | Umezu T | Year | 2021 |
| Journal | Biochem Biophys Res Commun | Volume | 582 |
| Pages | 111-117 | PubMed ID | 34710825 |
| Mgi Jnum | J:316329 | Mgi Id | MGI:6835695 |
| Doi | 10.1016/j.bbrc.2021.10.043 | Citation | Umezu T, et al. (2021) Smad2 and Smad3 expressed in skeletal muscle promote immobilization-induced bone atrophy in mice. Biochem Biophys Res Commun 582:111-117 |
| abstractText | Skeletal muscle is known to regulate bone homeostasis through muscle-bone interaction, although factors that control this activity remain unclear. Here, we newly established Smad3-flox mice, and then generated skeletal muscle-specific Smad2/Smad3 double conditional knockout mice (DcKO) by crossing Smad3-flox with skeletal muscle-specific Ckmm Cre and Smad2-flox mice. We show that immobilization-induced gastrocnemius muscle atrophy occurring due to sciatic nerve denervation was partially but significantly inhibited in DcKO mice, suggesting that skeletal muscle cell-intrinsic Smad2/3 is required for immobilization-induced muscle atrophy. Also, tibial bone atrophy seen after sciatic nerve denervation was partially but significantly inhibited in DcKO mice. Bone formation rate in wild-type mouse tibia was significantly inhibited by immobilization, but inhibition was abrogated in DcKO mice. We propose that skeletal muscle regulates immobilization-induced bone atrophy via Smad2/3, and Smad2/3 represent potential therapeutic targets to prevent both immobilization-induced bone and muscle atrophy. |
