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  • Title: Smad2 and Smad3 expressed in skeletal muscle promote immobilization-induced bone atrophy in mice.
    Author: Umezu T, Nakamura S, Sato Y, Kobayashi T, Ito E, Abe T, Kaneko M, Nomura M, Yoshimura A, Oya A, Matsumoto M, Nakamura M, Kanaji A, Miyamoto T.
    Journal: Biochem Biophys Res Commun; 2021 Dec 10; 582():111-117. PubMed ID: 34710825.
    Abstract:
    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.
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