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首页> 外文期刊>Cellular Physiology and Biochemistry >Neuronostatin Attenuates Myocardial Contractile Function through Inhibition of Sarcoplasmic Reticulum Ca2+-ATPase in Murine Heart
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Neuronostatin Attenuates Myocardial Contractile Function through Inhibition of Sarcoplasmic Reticulum Ca2+-ATPase in Murine Heart

机译：Neuronostatin通过抑制鼠心肌浆网Ca2 + -ATPase减弱心肌收缩功能。

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biBackground/Aims /i/bNeuronostatin, derived from the somatostatin preprohormone, was recently identified to be produced by several tissues exerting a role in cardiovascular regulation and metabolism. Nonetheless, the precise mechanism behind neuronostatin-elicited myocardial responses remains elusive. biMethods /i/bThis study was designed to elucidate the impact of neuronostatin on cardiac contractile function and the underlying mechanism of action involved. Adult male C57 BL/6 mice were subjected to a bolus injection of neuronostatin (50 μg/kg, i.p.). Echocardiographic, cardiomyocyte contractile and intracellular Casup2+/sup handling properties were monitored to evaluate the effect of neuronostatin on cardiac function. Western blot analysis was used to examine potential signaling mechanisms involved. biResults /i/bNeuronostatin administration suppressed myocardial and cardiomyocyte contractile function and disturbed intracellular Casup2+/sup homeostasis. We observed enlarged LVESD (with unchanged LVEDD), reduced fractional shortening, depressed peak shortening, maximal velocity of shortening/relengthening, resting and electrically-stimulated rise in intracellular Casup2+/sup, and prolonged relengthening duration in hearts from neuronostatin-treated mice. These effects were accompanied by downregulation of phosphorylation of sarcoplasmic reticulum Casup2+/sup-ATPase (SERCA) and phospholamban (PLB) and activation of AMPK. biConclusion /i/bOur data suggest that the cardiac depressant properties of neuronostatin possibly associated with loss of SERCA phosphorylation and AMPK activation. These findings revealed a potent inhibitory capacity for neuronostatin on cardiac function, the physiological relevance of which deserves further study.
机译：背景/目的 Neuronostatin来源于生长抑素前激素，最近被发现由在心血管调节和代谢中起作用的几种组织产生。尽管如此，神经抑制素引起的心肌反应背后的确切机制仍然难以捉摸。 方法 该研究旨在阐明神经抑素对心脏收缩功能的影响及其潜在的作用机制。成年雄性C57 BL / 6小鼠大剂量注射神经抑素（50μg/ kg，腹腔注射）。监测超声心动图，心肌细胞收缩和细胞内Ca 2 + 处理特性，以评估神经抑素对心脏功能的影响。蛋白质印迹分析用于检查涉及的潜在信号传导机制。 结果 神经调节素抑制心肌和心肌细胞的收缩功能，并破坏细胞内Ca 2 + 的体内稳态。我们观察到LVESD增大（LVEDD不变），缩短的分数缩短，降低的峰缩短，缩短/延长的最大速度，细胞内Ca 2 + 的静息和电刺激的上升以及延长的延长心脏持续时间来自神经抑素治疗的小鼠。这些作用伴随着肌浆网Ca 2 + -ATPase（SERCA）和phospholamban（PLB）磷酸化的下调以及AMPK的激活。 结论 我们的数据表明，神经抑素的心脏抑制特性可能与SERCA磷酸化和AMPK激活的丧失有关。这些发现揭示了神经抑制素对心脏功能的有效抑制能力，其生理相关性值得进一步研究。

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