Catecholamines modulate protein turnover in cultured, quiescent rabbit cardiac myocytes.
Catecholamines modulate protein turnover in cultured, quiescent rabbit cardiac myocytes.
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儿茶酚胺调节培养的静止兔心肌细胞中的蛋白质周转。
DOI：
10.1152/ajpheart.1993.265.1.h329
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Samarel,AM
中科院分区：
文献类型：
--
作者：
Decker,RS;Cook,MG;Behnke-Barclay,MM;Decker,ML;Lesch,M;Samarel,AM
当兔心室肌细胞培养1周，然后暴露于α-和/或β-肾上腺素能受体激动剂，这种非跳动的心脏细胞制剂公开增加蛋白质-DNA的比例和RNA含量升高，表明细胞肥大。去甲肾上腺素、异丙肾上腺素和苯肾上腺素引起肥大，去甲肾上腺素引起的反应大于异丙肾上腺素或苯肾上腺素。特定的α-和β-拮抗剂通过抑制儿茶酚胺诱导的蛋白质周转变化来阻断生长。每一个儿茶酚胺增强48小时内的蛋白质合成的分数率，然而，生长速度的变化似乎调制，在一定程度上，由蛋白质降解的改变。尽管总蛋白和肌动蛋白的合成速率与体内测量的值相似，但肌球蛋白重链合成的分数速率仅为体内水平的22%。双标记免疫荧光显微镜进一步说明，儿茶酚胺治疗加速这些静止的心脏细胞的肌原纤维破坏。这些观察结果表明，在跳动的情况下，收缩蛋白质周转的神经体液调制与维持肌原纤维的完整性，即使儿茶酚胺诱导细胞肥大。
When rabbit ventricular myocytes were cultured for 1 wk and then exposed to alpha- and/or beta-adrenergic agonists, such nonbeating heart cell preparations disclosed increased protein-to-DNA ratios and elevated RNA content, indicative of cellular hypertrophy. Norepinephrine, isoproterenol, and phenylephrine provoked hypertrophy with norepinephrine eliciting a greater response than isoproterenol or phenylephrine. Specific alpha- and beta-antagonists blocked growth by inhibiting catecholamine-induced changes in protein turnover. Each catecholamine enhanced the fractional rate of protein synthesis within 48 h; however, changes in growth rates appeared to be modulated, in part, by alterations in protein degradation. Even though rates of total protein and actin synthesis resembled values measured in vivo, myosin heavy chain fractional rate of synthesis was only 22% of in vivo levels. Double label immunofluorescence microscopy further illustrated that catecholamine treatment accelerated myofibrillar disruption in these quiescent heart cells. These observations suggested that in the absence of beating, neurohumoral modulation of contractile protein turnover was not associated with the maintenance of myofibrillar integrity even though catecholamines induced cellular hypertrophy.