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THE INTRINSIC DURABILITY OF AORTIC VALVE ECM IN ABSENCE OF CELLULAR MAINTENANCE

机译:缺乏细胞维持性时主动脉瓣ECM的内在耐用性

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Without cellular maintenance, AV leaflet fiber network became unfolded, stretched out. and thinned during simulated function for up to 4 weeks. We found that elastin fibers were absence in the flow loop exercised leaflets (Fig. 3). Note that elastin fibers were preserved in the static control that subjected to the same solution environment. Tt could be concluded that degradation along can not explain the absence of elastin in fatigued leaflets. We speculated that mechanical factors caused the loss of elastin fibers that lack of stabilizing crosslinks. The loss of elastin likely accelerated unfolding and straightening of collagen fibers. Mechanically, the structural alteration changed the reference status of fatigued tissue and resulted in a lower net tissue extensibility.We conclude that, in absence of cellular maintenance, decellularized valve leaflets experience rapid structural deterioration due to lack of exogenous stabilizing crosslinks and the structural disruption ss irreversible and cumulative. Apparently, recellularization is a key for the successful development of TEHV via decellularization approach.
机译:没有细胞维护,AV小叶纤维网络就无法展开,伸展。并在模拟功能期间减薄长达4周。我们发现运动循环的小叶中不存在弹性蛋白纤维(图3)。注意,弹性蛋白纤维被保存在经受相同溶液环境的静态对照中。可以得出这样的结论,即衰老不能解释疲劳的小叶中弹性蛋白的缺乏。我们推测,机械因素会导致缺乏稳定交联的弹性蛋白纤维损失。弹性蛋白的损失可能会加速胶原纤维的展开和拉直。在机械上,结构改变改变了疲劳组织的参考状态,并导致较低的净组织延伸性。 我们得出的结论是,在缺乏细胞维持的情况下,脱细胞的瓣膜小叶会由于缺乏外源性稳定交联和结构不可逆且不可逆的破坏而经历快速的结构恶化。显然,重新细胞化是通过脱细胞方法成功开发TEHV的关键。

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