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首页> 外文期刊>Communications in Agricultural and Applied Biological Sciences >PRIMARY HUMAN SKELETAL MYOBLAST CELLS FROM PATIENTS WITH CHRONIC HEART FAILURE EXHIBIT A DELAYED PROLIFERATIVE CAPACITY
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PRIMARY HUMAN SKELETAL MYOBLAST CELLS FROM PATIENTS WITH CHRONIC HEART FAILURE EXHIBIT A DELAYED PROLIFERATIVE CAPACITY

机译：患有慢性心力衰竭的患者的原代人骨骼肌成骨细胞表现出延迟的增殖能力

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摘要

Peripheral skeletal muscle wasting is observed in a variety of chronic diseases including chronic heart failure (CHF) (Conraads et al., 2008; Szabo et al., 2014; von Haehling et al., 2014). Muscle wasting is present in approximately 70% of CHF patients and confers poor prognosis (von Haehling et al., 2007; Loncar et al., 2013). Although a number of hypotheses have been put forth to explain the loss of skeletal muscle mass, the mechanisms that underlie CHF-related muscle wasting are currently not clear.Primary skeletal muscle cells retain the phenotypic and genotypic traits of the donor (Berggren et al., 2007; McAinch et al., 2007). As such, by using standard conditions, the in vitro culture of primary skeletal muscle myoblasts isolated from biopsy tissue of CHF patients is a promising tool to study muscle loss in these patients (Sente et al., 2014).The purpose of the present study was to evaluate the proliferative capacity of primary CHF myoblasts. First, we analyzed the kinetics of clonal growth over a ten-day period by phase contrast microscopy. Secondly, cellular impedance was dynamically assessed using a high resolution cell electronic sensing system (i.e. xCELLigence Real-Time Cellular Analysis (RTCA) detection platform).
机译：在包括慢性心力衰竭（CHF）在内的多种慢性疾病中均观察到周围骨骼肌的消瘦（Conraads等，2008; Szabo等，2014; von Haehling等，2014）。大约70％的CHF患者存在肌肉消耗，预后不良（von Haehling等，2007; Loncar等，2013）。尽管提出了许多假说来解释骨骼肌质量的损失，但目前尚不清楚CHF相关肌肉消瘦的基础机制。主要骨骼肌细胞保留了供体的​​表型和基因型特征（Berggren等。 ，2007; McAinch等，2007）。因此，通过使用标准条件，从CHF患者的活检组织中分离的原代骨骼肌成肌细胞的体外培养是研究这些患者肌肉损失的有前途的工具（Sente等人，2014）。目的是评估原发性CHF成肌细胞的增殖能力。首先，我们通过相差显微镜分析了为期十天的克隆生长动力学。其次，使用高分辨率细胞电子传感系统（即xCELLigence实时细胞分析（RTCA）检测平台）动态评估细胞阻抗。

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