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. 2014 Apr 1;3(4):e156. doi: 10.1038/mtna.2014.7

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Copyright © 2014 The American Society of Gene & Cell Therapy

Molecular Therapy-Nucleic Acids is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/

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ALK5 antisense oligonucleotides (AONs) inhibit MSTN and transforming growth factor-β (TGF-β) signaling. (a) ALK5 AONs (200 nmol/l) specifically repressed TGF-β-induced (CAGA)₁₂-luciferase activity in both C2C12 myoblasts and C3H10T1/2 cells. (b) MSTN-induced Smad3-dependent (CAGA)₁₂-luciferase activity was specifically repressed by ALK5 AONs (200 nmol/l) in C3H10T1/2 mesenchymal stem cells. In contrast, ALK5 AONs did not inhibit MSTN activity in C2C12 myoblasts. Firefly luciferase activity of (CAGA)₁₂-luciferase constructs was corrected with renilla-luciferase activity of cotransfected cytomegalovirus-renilla constructs. The experiments were performed at least three times and each experiment was performed in triplicate. The values were averaged and plotted as fold relative to control AON (Ctrl AON)-transfected samples. Error bars represent standard deviations. *P < 0.05, **P < 0.01.