• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文会议>International Conference on Cancer Care Informatics >Motor Neuron-Skeletal Muscle Co Culture Model: A Potential Novel in Vitro and Computaional Platform to Investigate Cancer Cachexia
【24h】

Motor Neuron-Skeletal Muscle Co Culture Model: A Potential Novel in Vitro and Computaional Platform to Investigate Cancer Cachexia

机译：运动神经元肌肉CO培养模型：潜在的新型体外和计算平台调查癌症恶棍

获取原文
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Skeletal muscle is the largest organs in the human body, comprising approximately 45% of total body weight. It is a primary site for glucose uptake (75% uptake) and storage (85%). The connection between motor neuron and skeletal muscle is the crucial final link in the human motor system controlling voluntary muscular movements. Consequently, muscle denervation and re-innervation dramatically alter muscle physiology. Vice versa, there is increasing evidence that muscle-dependent trophic, cell adhesion, and axon-guidance signals play an essential role in the formation and maintenance of the neuromuscular junction. Therefore, muscle loss and damage (wasting) lead to various significant negative health consequences as in diabetes, cardiovascular disease and cancer cachexia. Cancer cachexia (CC) is a muscle wasting syndrome characterised by significant weight loss. Cancer cachectic patients experience numerous complications including, but not limited to, reduced effectiveness of chemotherapy, reduced mobility and reduced functionality of muscle-dependent systems, such as the respiratory and cardiovascular systems, leading to decreased quality of life and survival. More than half of cancer patients suffer from cachexia, and strikingly, nearly one-third of cancer deaths are related to cachexia rather than the tumour burden. Despite many decades of extensive animal studies, underlying mechanisms of cancer cachexia are still poorly defined and therapeutic options are limited. This is largely due to that animal models do not entirely reflect disease progression and complexity in humans. Furthermore, typical in vitro models of CC are generally established using animal derived cells and/or the use of skeletal muscle cell monolayer cultures, that fail to mimic in vivo conditions, particularly due to the lack of functional innervation/contraction. Thus, the development of new models to study and manipulate cancer cachexia has the potential to provide significant insight into mechanism underlying CC. In this study, we develop a novel in vitro co-culture model utilising human embryonic stem cells (hESCs)-derived motor neuron and immortalised human myoblasts to allow us to investigate cancer cachexia pathophysiology. This unique serum- and trophic factor-free co-culture provides a tool to study vital features of CC, will expand the understanding of the underlying mechanisms and will allow a more reliable evaluation of prospective chemotherapy drugs for translational purposes.
机译：骨骼肌是人体中最大的器官，包含总体重的约45％。它是葡萄糖摄取（75％摄取）和储存的主要部位（85％）。电机神经元和骨骼肌之间的连接是控制自愿肌肉运动的人机系统中的主要链路。因此，肌肉消除和重新检查显着改变肌肉生理学。反之亦然，有越来越多的证据表明肌肉依赖性营养，细胞粘附和轴突 - 引导信号在神经肌肉交叉点的形成和维持中起重要作用。因此，肌肉损失和损害（浪费）导致各种显着的负面健康后果，如糖尿病，心血管疾病和癌症恶病症。癌症恶病毒（CC）是一种肌肉浪费综合征，其特征在于重量损失显着。癌症遗传患者体验着许多并发症，包括但不限于减少化疗的有效性，降低肌肉依赖性系统（例如呼吸和心血管系统）的减少和减少功能，导致生命质量和生存率降低。超过一半的癌症患者患有恶肠病，并且令人惊讶的是，近三分之一的癌症死亡与恶病症有关，而不是肿瘤负担。尽管数十年的广泛的动物研究，但癌症恶化的潜在机制仍然是明确的，治疗选择有限。这主要是由于动物模型并不完全反映人类的疾病进展和复杂性。此外，CC的典型体外模型通常使用动物衍生的细胞和/或使用骨骼肌细胞单层培养物，其未能在体内条件下模仿，特别是由于缺乏功能性接头/收缩。因此，开发用于研究和操纵癌症恶化的新模型有可能对CC潜在的机制提供显着的洞察力。在这项研究中，我们开发了利用人胚胎干细胞（HESC）的运动神经元和永生化的人肌细胞，允许我们调查癌症恶魔病理生理学的一种新型的体外共培养模型。这种独特的血清和营养因子无因素的共同文化提供了一种研究CC的重要特征的工具，将扩大对潜在机制的理解，并将对前瞻性化疗药物进行更可靠的评估，以进行翻译目的。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号