Application of myogenetic oligodeoxynucleotide to diabetic skeletal muscle myoblasts

Application of myogenetic oligodeoxynucleotide to diabetic skeletal muscle myoblasts

Shunichi Nakamura1, Koji Umezawa1,2, Shinichi Yonekura1,2, Takeshi Shimosato1,2, Tomohide Takaya1,2.

  1. Graduate School of Science and Technology, Shinshu University.
  2. Institute for Biomedical Sciences, Shinshu University.

日本核酸医薬学会第5回年会 (大阪), 2019/07/11 (口演/ポスター).


Homeostasis of skeletal muscle is maintained by myogenic progenitors called myoblasts. We recently identified a telomeric 18 nt-oligodeoxynucleotide, myoDN, which intensively facilitates myogenic differentiation. myoDN induces differentiation of myoblasts, rhabdomyosarcoma, and pluripotent stem cells in a structure-dependent manner. In this study, we investigated the applicability of myoDN to diabetic muscle atrophy. Hyperglycemia attenuates myoblast differentiation and causes muscle atrophy. We have indicated that high-glucose concentration deteriorates myoblast differentiation. In this study, we compared myoblast differentiation of healthy and diabetic subjects, and examined the effects of myoDN on diabetic myoblasts. The myoblasts isolated from healthy and diabetic subjects were induced differentiation with 10 uM myoDN for 48 h. Myogenic differentiation was quantified by immunostaining for myosin heavy chain (MHC). In myoDN(-) group, MHC+ cells were markedly decreased in diabetic myoblasts compared to healthy myoblasts, indicating that diabetes attenuates myoblast differentiation. On the other hand, myoDN significantly increased MHC+ cells in both healthy and diabetic myoblasts compared to myoDN(-) group. It demonstrates that myoDN can recover the myogenic differentiation attenuated in diabetes. myoDN will be useful for prevention and therapy of diabetic muscle atrophy.