Cited by 25Muscle Physiology and DisordersCongenital heart defects researchPluripotent Stem Cells Research

Tetrahydropalmatine Promotes Myoblast Differentiation through Activation of p38MAPK and MyoD

Lee, Sang-Jin, Yoo, Miran, Go, Ga-Yeon, Hwang, Jeongmi, Lee, Hyo-Gun, Kim, Yong-Kee, Seo, Dong-Wan, Baek, Nam-In +3 more·2014·Biochemical and Biophysical Research Communications

Abstract

Myoblast differentiation is fundamental to the development and regeneration of skeletal muscle after injury or disease. MyoD family transcription factors play a key role to promote myoblast differentiation. In a screen for MyoD activators, we identified tetrahydropalmatine (THP), a natural compound isolated from Corydalis turtschaninovii. The treatment of C2C12 myoblasts with THP enhanced the level of MyoD, Myogenin and myosin heavy chain (MHC) proteins and the formation of larger multinucleated myotubes, compared to the control treatment. The THP treatment dramatically enhanced the activities of p38MAPK and Akt, the key promyogenic kinases which activate MyoD. The enhanced myoblast differentiation by THP treatment can be blocked by inhibition of p38MAPK or Akt by SB203580 or LY294002, respectively. In addition, THP treatment restored myotube formation of Cdo-depleted C2C12 cells through activation of p38MAPK. Moreover, THP enhanced the efficiency of trans-differentiation of 10T1/2 fibroblasts into myoblasts mediated by MyoD. These results indicate that THP has a promyogenic effect by upregulation of p38MAPK and Akt resulting in enhanced MyoD activation. Our findings suggest that THP has a potential as a therapeutic candidate to prevent fibrosis and improve muscle regeneration and repair.

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Crossref · 10.1016/j.bbrc.2014.10.115

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  • Tetrahydropalmatine enhances myoblast differentiation through the activation of p38MAPK and MyoD and has potential as a therapeutic candidate to prevent fibrosis and improve muscle regeneration and repair in C2C12 myotubes.

    “Tetrahydropalmatine, another compound isolated from Corydalis turtschaninovii, enhances myoblast differentiation through the activation of p38MAPK and MyoD and has the potential as a therapeutic candidate to prevent fibrosis and improve muscle regeneration and repair in C2C12 myotubes [135].”
  • MyoD activity is regulated by promyogenic signaling pathways including p38 MAPK and Akt.

    “The activity of MyoD is regulated by promyogenic signaling pathways which include p38 mitogen-activated protein kinase (p38 MAPK) and Akt [5, 7, 8].”

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Authors
Lee, S.-J., Yoo, M., Go, G.-Y., Hwang, J., Lee, H.-G., Kim, Y.-K., Seo, D.-W., Baek, N.-I., Ryu, J.-H., Kang, J.-S., & Bae, G.-U.
Affiliations
  • Sookmyung Women's University (KR)
  • Dankook University (KR)
  • Kyung Hee University (KR)
  • Samsung Biomedical Research Institute (KR)
Venue
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Published
2014-12
Volume
455
Issue
3-4
Pages
147-152
ISSN
0006-291X (ISSN-L)
OpenAlex
W2031847565
Cited by
25
References
20
Citations by year
2026: 1 · 2025: 1 · 2022: 3 · 2021: 2 · 2020: 5 · 2019: 2 · 2018: 3 · 2017: 3 · 2016: 4 · 2015: 1
FWCI
1.09
Type
journal article
Language
en
Open access
closed
Locations
  • Biochemical and Biophysical Research Communications (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Research Foundation of Korea
  • Korea government (2011-0030074)
  • Sookmyung Women’s University (1-1103-0651)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pluripotent Stem Cells Research
Keywords
tetrahydropalmatine, myogenesis, p38 MAPK, MyoD, Akt, C2C12 myoblasts, myotube formation, skeletal muscle regeneration, CdO, myogenic transcription factors, natural compounds
MeSH terms
Animals, Berberine Alkaloids, Cell Communication, Cell Differentiation, Chromones, Enzyme Activation, Fibroblasts, Fibrosis, Imidazoles, Morpholines, Pyridines, Regeneration, Signal Transduction, Gene Expression Regulation, Enzymologic, MyoD Protein, Myogenin, Myoblasts, p38 Mitogen-Activated Protein Kinases, Mice, Sarcopenia

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