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来自核心蛋白聚糖和双糖链蛋白聚糖基因敲除小鼠模型的跟腱,其力学和结构特性低于基于图像的经验损伤模型所预测的水平。

Achilles tendons from decorin- and biglycan-null mouse models have inferior mechanical and structural properties predicted by an image-based empirical damage model.

作者信息

Gordon J A, Freedman B R, Zuskov A, Iozzo R V, Birk D E, Soslowsky L J

机构信息

McKay Orthopaedic Research Laboratory, University of Pennsylvania, Philadelphia, PA, USA.

Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USA.

出版信息

J Biomech. 2015 Jul 16;48(10):2110-5. doi: 10.1016/j.jbiomech.2015.02.058. Epub 2015 Mar 31.

DOI:10.1016/j.jbiomech.2015.02.058
PMID:25888014
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4492865/
Abstract

Achilles tendons are a common source of pain and injury, and their pathology may originate from aberrant structure function relationships. Small leucine rich proteoglycans (SLRPs) influence mechanical and structural properties in a tendon-specific manner. However, their roles in the Achilles tendon have not been defined. The objective of this study was to evaluate the mechanical and structural differences observed in mouse Achilles tendons lacking class I SLRPs; either decorin or biglycan. In addition, empirical modeling techniques based on mechanical and image-based measures were employed. Achilles tendons from decorin-null (Dcn(-/-)) and biglycan-null (Bgn(-/-)) C57BL/6 female mice (N=102) were used. Each tendon underwent a dynamic mechanical testing protocol including simultaneous polarized light image capture to evaluate both structural and mechanical properties of each Achilles tendon. An empirical damage model was adapted for application to genetic variation and for use with image based structural properties to predict tendon dynamic mechanical properties. We found that Achilles tendons lacking decorin and biglycan had inferior mechanical and structural properties that were age dependent; and that simple empirical models, based on previously described damage models, were predictive of Achilles tendon dynamic modulus in both decorin- and biglycan-null mice.

摘要

跟腱是疼痛和损伤的常见来源,其病理可能源于异常的结构功能关系。富含亮氨酸的小分子蛋白聚糖(SLRPs)以肌腱特异性方式影响力学和结构特性。然而,它们在跟腱中的作用尚未明确。本研究的目的是评估在缺乏I类SLRPs(核心蛋白聚糖或双糖链蛋白聚糖)的小鼠跟腱中观察到的力学和结构差异。此外,还采用了基于力学和图像测量的经验建模技术。使用了来自核心蛋白聚糖基因敲除(Dcn(-/-))和双糖链蛋白聚糖基因敲除(Bgn(-/-))的C57BL/6雌性小鼠的跟腱(N = 102)。每条跟腱都进行了动态力学测试方案,包括同步偏振光图像采集,以评估每条跟腱的结构和力学特性。一种经验损伤模型被改编用于遗传变异,并与基于图像的结构特性一起用于预测肌腱的动态力学特性。我们发现,缺乏核心蛋白聚糖和双糖链蛋白聚糖的跟腱具有较差的力学和结构特性,且这些特性与年龄有关;并且基于先前描述的损伤模型的简单经验模型能够预测核心蛋白聚糖基因敲除和双糖链蛋白聚糖基因敲除小鼠跟腱的动态模量。

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