Dehydrocorydaline promotes myogenic differentiation via p38 MAPK activation

Yoo,Miran; Lee,Sang‑Jin; Kim,Yong  Kee; Seo,Dong‑Wan; Baek,Nam‑In; Ryu,Jae‑Ha; Kang,Jong‑Sun; Bae,Gyu‑Un

doi:10.3892/mmr.2016.5653

Dehydrocorydaline promotes myogenic differentiation via p38 MAPK activation

Authors:
- Miran Yoo
- Sang‑Jin Lee
- Yong Kee Kim
- Dong‑Wan Seo
- Nam‑In Baek
- Jae‑Ha Ryu
- Jong‑Sun Kang
- Gyu‑Un Bae
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Affiliations: Research Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul 140‑742, Republic of Korea, Department of Biochemistry, College of Pharmacy, Dankook University, Cheonan, Chungcheongnam 330‑714, Republic of Korea, Department of Oriental Medicine, The Graduate School of Biotechnology, Institute of Life Sciences & Resources, Kyung Hee University, Yongin, Gyeonggi 446‑701, Republic of Korea, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, Gyeonggi 440‑746, Republic of Korea
Published online on: August 19, 2016 https://doi.org/10.3892/mmr.2016.5653
Pages: 3029-3036
Copyright: © Yoo et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Muscle regeneration is a coordinated process that involves proliferation and differentiation of muscle progenitor cells. Activation of MyoD is a key event in myogenic differentiation, which is regulated by p38 mitogen‑activated protein kinases (MAPK). In a screen of natural compounds for the enhancement of MyoD activity, dehydrocorydaline (DHC) from the Corydalis tuber was identified. Treatment of C2C12 myoblasts with DHC increased the expression levels of muscle‑specific proteins, including MyoD, myogenin and myosin heavy chain. In addition, C2C12 myoblasts exhibited enhanced multinucleated myotube formation without any cytotoxicity. Treatment with DHC elevated p38 MAPK activation and the interaction of MyoD with an E protein, which is likely to result in activation of MyoD and promotion of myoblast differentiation. Furthermore, defects in differentiation‑induced p38 MAPK activation and myoblast differentiation induced by depletion of the promyogenic receptor protein Cdo in C2C12 myoblasts were restored by DHC treatment. In conclusion, these results indicated that DHC stimulates p38 MAPK activation, which can enhance heterodimerization of MyoD and E proteins, thus resulting in MyoD activation and myoblast differentiation. These findings suggested that DHC may be considered a potential therapeutic compound for the improvement of muscle stem cell regenerative capacity in injured muscle.

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