Evidence map›Paper›PMID 27573543›Full record

ArticleMolecular medicine reports2016

Dehydrocorydaline promotes myogenic differentiation via p38 MAPK activation.

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

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Miran YooResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul 140‑742, Republic of Korea.
Sang-Jin LeeResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul 140‑742, Republic of Korea.
Yong Kee KimResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul 140‑742, Republic of Korea.
Dong-Wan SeoDepartment of Biochemistry, College of Pharmacy, Dankook University, Cheonan, Chungcheongnam 330‑714, Republic of Korea.
Nam-In BaekDepartment of Oriental Medicine, The Graduate School of Biotechnology, Institute of Life Sciences & Resources, Kyung Hee University, Yongin, Gyeonggi 446‑701, Republic of Korea.
Jae-Ha RyuResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul 140‑742, Republic of Korea.
Jong-Sun KangDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon, Gyeonggi 440‑746, Republic of Korea.
Gyu-Un BaeResearch Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul 140‑742, Republic of Korea.
Sookmyung Women's University · KRDankook University · KRKyung Hee University · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AlkaloidsAnimalsCell LineCorydalisDrugs, Chinese HerbalEnzyme ActivationMiceMuscle DevelopmentMyoblastsMyoD Proteinp38 Mitogen-Activated Protein KinasesAlkaloidsdehydrocorydalinDrugs, Chinese HerbalMyoD1 myogenic differentiation proteinMyoD Proteinp38 Mitogen-Activated Protein Kinases

Identifiers

PMID27573543
PMCPMC5042734
OpenAlexW2517473046

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.