McArdle Laboratory for Cancer Research, Department of Oncology, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.
PLoS One. 2010 Nov 30;5(11):e15511. doi: 10.1371/journal.pone.0015511.
Transforming growth factor beta 1 (TGF-β1) is an inhibitor of muscle cell differentiation that is associated with fibrosis, poor regeneration and poor function in some diseases of muscle. When neutralizing antibodies to TGF-β1 or the angiotensin II inhibitor losartan were used to reduce TGF-β1 signaling, muscle morphology and function were restored in mouse models of Marfan Syndrome and muscular dystrophy. The goal of our studies was to identify additional agents that overcome the anti-myogenic effect of TGF-β1.
METHODOLOGY/PRINCIPAL FINDINGS: A high-content cell-based assay was developed in a 96-well plate format that detects the expression of myosin heavy chain (MHC) in C2C12 cells. The assay was used to quantify the dose-dependent responses of C2C12 cell differentiation to TGF-β1 and to the TGF-β1 Type 1 receptor kinase inhibitor, SB431542. Thirteen agents previously described as promoting C2C12 differentiation in the absence of TGF-β1 were screened in the presence of TGF-β1. Only all-trans retinoic acid and 9-cis retinoic acid allowed a maximal level of C2C12 cell differentiation in the presence of TGF-β1; the angiotensin-converting enzyme inhibitor captopril and 10 nM estrogen provided partial rescue. Vitamin D was a potent inhibitor of retinoic acid-induced myogenesis in the presence of TGF-β1. TGF-β1 inhibits myoblast differentiation through activation of Smad3; however, retinoic acid did not inhibit TGF-β1-induced activation of a Smad3-dependent reporter gene in C2C12 cells.
CONCLUSIONS/SIGNIFICANCE: Retinoic acid alleviated the anti-myogenic effect of TGF-β1 by a Smad3-independent mechanism. With regard to the goal of improving muscle regeneration and function in individuals with muscle disease, the identification of retinoic acid is intriguing in that some retinoids are already approved for human therapy. However, retinoids also have well-described adverse effects. The quantitative, high-content assay will be useful to screen for less-toxic retinoids or combinations of agents that promote myoblast differentiation in the presence of TGF-β1.
转化生长因子-β1(TGF-β1)是一种肌细胞分化抑制剂,与纤维化、再生不良和某些肌肉疾病的功能不良有关。当使用中和转化生长因子-β1的抗体或血管紧张素 II 抑制剂洛沙坦来降低 TGF-β1 信号时,马凡综合征和肌肉营养不良的小鼠模型中的肌肉形态和功能得到了恢复。我们研究的目标是确定其他能够克服 TGF-β1 抗肌生成作用的药物。
方法/主要发现:开发了一种基于 96 孔板格式的高内涵细胞测定法,用于检测 C2C12 细胞中肌球蛋白重链(MHC)的表达。该测定法用于定量检测 C2C12 细胞分化对 TGF-β1 和 TGF-β1 型 1 受体激酶抑制剂 SB431542 的剂量依赖性反应。以前描述的 13 种在没有 TGF-β1 的情况下促进 C2C12 分化的药物在 TGF-β1 存在的情况下进行了筛选。只有全反式视黄酸和 9-顺式视黄酸允许 C2C12 细胞在 TGF-β1 存在的情况下达到最大分化水平;血管紧张素转换酶抑制剂卡托普利和 10 nM 雌激素提供部分挽救。维生素 D 是 TGF-β1 存在时视黄酸诱导的肌生成的有效抑制剂。TGF-β1 通过激活 Smad3 抑制成肌细胞分化;然而,视黄酸并没有抑制 C2C12 细胞中 Smad3 依赖性报告基因的 TGF-β1 诱导激活。
结论/意义:视黄酸通过 Smad3 非依赖性机制缓解了 TGF-β1 的抗肌生成作用。就改善患有肌肉疾病的个体的肌肉再生和功能的目标而言,视黄酸的鉴定很有趣,因为一些视黄酸已经被批准用于人类治疗。然而,视黄酸也有很好描述的不良反应。该定量、高内涵测定法将有助于筛选出毒性较小的视黄酸或在 TGF-β1 存在下促进成肌细胞分化的药物组合。