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甲状腺素致心肌细胞肥大的机制探讨 被引量:2

Mechanisms of Cardiomyocytes Hypertrophy Induced by Thyroid Hormone
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摘要 目的:探讨甲状腺素致心肌细胞肥大的相关机制。方法:取分离培养的乳鼠心肌细胞,用L-甲状腺素(T3)诱导心肌细胞肥大,然后再加入磷脂酰肌醇-3-激酶(PI3-K)抑制剂LY294002和哺乳动物雷帕霉素靶蛋白(mTOR)特异性抑制剂雷帕霉素进行干预;采用测量心肌细胞表面积及3H-亮氨酸掺入、Western blot等检测方法。结果:甲状腺素诱导的心肌细胞肥大能被LY294002或雷帕霉素抑制,LY294002能抑制甲状腺素激活丝氨酸/苏氨酸激酶(AKT)和mTOR,雷帕霉素能特异性阻断mTOR的活化。结论:甲状腺素能通过PI3-K/Akt-mTOR信号通路促进心肌细胞肥大。 Objective:To investigate the mechanisms of cardiac myocytes hypertrophy induced by thyroid hormone.Methods:The cultured cardiomyocytes in vitro were used for experiments.The hypertrophic myocytes were induced by L-thyroxine.Phosphatidylinositol 3'-kinase(PI3-K)inhibitor LY294002and mammalian target of rapamycin(mTOR)inhibitor rapamycin were also employed to detect the underlying mechanism.The measurement of cell surface area,3 H-leucine incorporation and Western blot were the major methods used in the experiment.Results:The L-thyroxine-induced cardiac myocytes hypertrophy was attenuated by LY294002or rapamycin,LY294002inhibited serine/threonine protein kinase(AKT)and mTOR activation induced by L-thyroxine and rapamycin specific inhibited mTOR phosphorylation.Conclusion:The L-thyroxine induces cardiomyocytes hypertrophy via the PI3-K/Akt-mTOR pathway.
出处 《武汉大学学报(医学版)》 CAS 北大核心 2010年第6期759-762,共4页 Medical Journal of Wuhan University
关键词 甲状腺素 心肌细胞肥大 信号转导分子 Thyroxine Cardiomyocytes Hypertrophy Signal Transduction Molecule
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