Hypertrophic cardiomyopathy occurs along with pathological phenomena such as cardiac hypertrophy, myocardial fibrosis and cardiomyocyte activity. However, few of the specific molecular mechanisms underlying this pathological condition have been mentioned. All target proteins and markers expression in the study was verified by PCR and western bloting. H9c2 cell morphology and behavior were analyzed using immunofluorescent and proliferation assays, respectively. And, the CTGF protein secreted in cell culture medium was detected by ELISA. We found that high expression of CTGF and low expression of EGFR were regulated by ERK1/2 signaling pathway during the cardiac hypertrophy induced by Ang-II stimulation. CTGF interacted with EGFR, and the interaction is reduced with the stimulation of Ang-II. ERK1/2 serves as the center of signal control during the cardiac hypertrophy. The ERK1/2 cooperates with GPCR and EGFR signaling, and promotes the occurrence and development of cardiac hypertrophy by regulating the expression and binding states of CTGF and EGFR. The study revealed a regulation model based on ERK1/2, suggesting that ERK1/2 signaling pathway may be an important control link for mitigation of hypertrophic cardiomyopathy treatment.

中文翻译：

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ERK1 / 2传达GPCR和EGFR信号传导途径，以促进Ang-II刺激下CTGF介导的肥厚型心肌病

肥厚型心肌病与诸如心肌肥大，心肌纤维化和心肌细胞活性之类的病理现象一起发生。但是，很少提及这种病理状态的具体分子机制。通过PCR和western blotting验证了研究中所有靶蛋白和标志物的表达。分别使用免疫荧光和增殖测定法分析了H9c2细胞的形态和行为。并且，通过ELISA检测细胞培养基中分泌的CTGF蛋白。我们发现在Ang-II刺激引起的心肌肥大过程中，ERK1 / 2信号传导通路调节CTGF​​的高表达和EGFR的低表达。CTGF与EGFR相互作用，并且在Ang-II刺激下相互作用减弱。ERK1 / 2是心脏肥大过程中信号控制的中心。ERK1 / 2与GPCR和EGFR信号传导协同作用，并通过调节CTGF​​和EGFR的表达和结合状态促进心脏肥大的发生和发展。该研究揭示了一种基于ERK1 / 2的调节模型，表明ERK1 / 2信号通路可能是缓解肥厚型心肌病治疗的重要控制环节。