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首页> 外文会议>2014 40th Annual Northeast Bioengineering Conference >Enhancing cell recruitment onto crosslinked fibrin microthreads with hepatocyte growth factor
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Enhancing cell recruitment onto crosslinked fibrin microthreads with hepatocyte growth factor

机译：用肝细胞生长因子增强细胞募集到交联的纤维蛋白微丝上

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Volumetric muscle loss (VML) defects caused by major trauma lead to loss of muscle mass, mobility, and ultimately may result in tissue morbidity. These large-scale injuries destroy native tissue structures such as the basal lamina, which serves as a regenerative template for muscle regeneration. Our approach to the regeneration of VML injuries is to use fibrin microthreads, scaffolds with similar morphology to native muscle, and modulate their mechanical and structural properties to recapitulate cues lost with the destruction of native tissue structures. In this study, we investigated the effect of adsorbing hepatocyte growth factor (HGF) onto crosslinked microthreads on myoblast proliferation and recruitment in an in vitro model designed to mimic in vivo satellite cell recruitment and found that active HGF is released for 1-2 days and is capable of stimulating myoblast migration in both 2D and 3D models. These data suggest that HGF-adsorbed microthreads can recruit myoblasts to the wound site, ultimately leading to an enhanced regenerative response in VML injuries.
机译：由重大创伤引起的体积性肌肉丢失（VML）缺陷会导致肌肉质量，活动性丧失，并最终可能导致组织发病。这些大规模的伤害破坏了天然组织结构，例如基底层，它是肌肉再生的再生模板。我们再生VML损伤的方法是使用纤维蛋白微丝，具有与天然肌肉相似形态的支架，并调节其机械和结构特性，以概括由于破坏天然组织结构而丢失的线索。在这项研究中，我们研究了在体外模拟体内卫星细胞募集的体外模型中，在交联微线上吸附肝细胞生长因子（HGF）对成肌细胞增殖和募集的影响，发现活性HGF释放了1-2天，能够在2D和3D模型中刺激成肌细胞迁移。这些数据表明，HGF吸附的微线可以将成肌细胞募集到伤口部位，最终导致VML损伤的再生反应增强。

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