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Dehydrocorydaline promotes myogenic differentiation via p38 MAPK activationopen access

Authors
Yoo, MiranLee, Sang-JinKim, Yong KeeSeo, Dong-WanBaek, Nam-InRyu, Jae-HaKang, Jong-SunBae, Gyu-Un
Issue Date
Oct-2016
Publisher
SPANDIDOS PUBL LTD
Keywords
Corydalis tuber; dehydrocorydaline; myoblast differentiation; MyoD; p38 MAPK
Citation
MOLECULAR MEDICINE REPORTS, v.14, no.4, pp.3029 - 3036
Journal Title
MOLECULAR MEDICINE REPORTS
Volume
14
Number
4
Start Page
3029
End Page
3036
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/3246
DOI
10.3892/mmr.2016.5653
ISSN
1791-2997
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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