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表儿茶素引发依赖MyoD的成肌细胞分化和成纤维细胞的肌源性转化。

Epicatechin elicits MyoD-dependent myoblast differentiation and myogenic conversion of fibroblasts.

作者信息

Lee Sang-Jin, Leem Young-Eun, Go Ga-Yeon, Choi Younhee, Song Yoo Jin, Kim Insol, Kim Do Yoon, Kim Yong Kee, Seo Dong-Wan, Kang Jong-Sun, Bae Gyu-Un

机构信息

Research Center for Cell Fate Control, College of Pharmacy, Sookmyung Women's University, Seoul, Republic of Korea.

Department of Molecular Cell Biology, Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea.

出版信息

PLoS One. 2017 Apr 6;12(4):e0175271. doi: 10.1371/journal.pone.0175271. eCollection 2017.

DOI:10.1371/journal.pone.0175271
PMID:28384253
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5383328/
Abstract

Prevention of age-associated reduction in muscle mass and function is required to manage a healthy life. Supplemental (-)-Epicatechin (EC) appears to act as a potential regulator for muscle growth and strength. However, its cellular and molecular mechanisms as a potential muscle growth agent have not been studied well. In the current study, we investigated a role of EC in differentiation of muscle progenitors to gain the molecular insight into how EC regulates muscle growth. EC enhanced myogenic differentiation in a dose-dependent manner through stimulation of promyogenic signaling pathways, p38MAPK and Akt. EC treatment elevated MyoD activity by enhancing its heterodimerization with E protein. Consistently, EC also positively regulated myogenic conversion and differentiation of fibroblasts. In conclusion, EC has a potential as a therapeutic or nutraceutical remedy to treat degenerative muscle diseases or age-related muscle weakness.

摘要

预防与年龄相关的肌肉质量和功能下降是维持健康生活所必需的。补充（-）-表儿茶素（EC）似乎是肌肉生长和力量的潜在调节剂。然而，其作为潜在肌肉生长剂的细胞和分子机制尚未得到充分研究。在本研究中，我们研究了EC在肌肉祖细胞分化中的作用，以深入了解EC如何调节肌肉生长的分子机制。EC通过刺激促肌生成信号通路p38MAPK和Akt，以剂量依赖的方式增强肌源性分化。EC处理通过增强MyoD与E蛋白的异源二聚化来提高其活性。同样，EC也对成纤维细胞的肌源性转化和分化起到正向调节作用。总之，EC有潜力作为治疗退行性肌肉疾病或与年龄相关的肌肉无力的治疗药物或营养补充剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ca/5383328/674f5578792f/pone.0175271.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ca/5383328/d4dbb61c453e/pone.0175271.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ca/5383328/0e102b7f6a76/pone.0175271.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ca/5383328/c7afada60392/pone.0175271.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ca/5383328/a24cd1e004a1/pone.0175271.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ca/5383328/674f5578792f/pone.0175271.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ca/5383328/d4dbb61c453e/pone.0175271.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ca/5383328/0e102b7f6a76/pone.0175271.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ca/5383328/c7afada60392/pone.0175271.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ca/5383328/a24cd1e004a1/pone.0175271.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57ca/5383328/674f5578792f/pone.0175271.g005.jpg

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