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首页> 外文期刊>Gene Therapy and Molecular Biology >Differential expression of 14-3-3ε duringphysiological, pathological cardiac hypertrophy andchronic heart failure in mice
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Differential expression of 14-3-3ε duringphysiological, pathological cardiac hypertrophy andchronic heart failure in mice

机译：小鼠生理，病理性心脏肥大和慢性心力衰竭期间14-3-3ε的差异表达

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Physiological cardiac hypertrophy associated with regular exercise is usually beneficial, in marked contrast topathological hypertrophy associated with disease. 14-3-3 proteins play a critical antiapoptotic function in cardiomyocytes. Whether it or other genes activated in the athlete’s heart might have an impact on cardiac function and survival in a setting of heart failure is unknown. To examine whether different changes of 14-3-3 proteins expression in physiological cardiac hypertrophy, pathological cardiac hypertrophy and chronic heart failure (CHF), we constructed mouse models of physiological cardiac hypertrophy to swim training, pathological cardiac hypertrophy to transverse aortic constriction (TAC) for 4 weeks and chronic heart failure to TAC for 16 weeks. In response to swimming training and TAC, mice showed significant increases in left ventricular diastolic posterior wall thickness (LVPWd), heart weight and normalized heart weight to body weight ratio. However, in CHF mice, LVPWd decreased, end-diastolic volume (EDV) increased and marked cardiac fibrosis was formed. Thus, pressure overload induced decompensate heart failure and eccentric hypertrophy. Moreover, 14-3-3ε protein expression of hearts was increased in response to swimming training but decreased in CHF mice. However, other isoforms (β, ζ) of 14-3-3 proteins were no obvious changes in these three models. Therefore, our results suggest that the expressions of 14-3-3ε are different in physiological and pathological hypertrophy, which may provide a potential gene strategy for the treatment of heart failure.
机译：与定期运动有关的生理性心脏肥大通常是有益的，这与与疾病有关的病理性肥大形成鲜明对比。 14-3-3蛋白在心肌细胞中起着至关重要的抗凋亡作用。目前尚不清楚该基因或运动员心脏中激活的其他基因是否会影响心脏功能，以及在发生心力衰竭时的存活率。为了检查生理性心脏肥大，病理性心脏肥大和慢性心力衰竭（CHF）中14-3-3蛋白表达的不同变化，我们构建了生理性心脏肥大的小鼠模型以进行游泳训练，病理性心脏肥大至横动脉主动脉缩窄（TAC） ）持续4周，而慢性心力衰竭至TAC持续16周。响应游泳训练和TAC，小鼠显示左心室舒张后壁厚度（LVPWd），心脏重量和标准化心脏重量与体重之比显着增加。但是，在CHF小鼠中，LVPWd降低，舒张末期容积（EDV）升高，并形成明显的心脏纤维化。因此，压力超负荷引起的代偿性心力衰竭和离心性肥大。此外，心脏的14-3-3ε蛋白表达响应游泳训练而增加，但在CHF小鼠中降低。但是，在这三个模型中，14-3-3蛋白的其他同工型（β，ζ）没有明显变化。因此，我们的结果表明14-3-3ε的表达在生理性和病理性肥大中是不同的，这可能为治疗心力衰竭提供了潜在的基因策略。

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