Improved biomechanical and biological outcomes in the MRL/MpJ murine strain following a full-length patellar tendon injury.

Improved biomechanical and biological outcomes in the MRL/MpJ murine strain following a full-length patellar tendon injury.
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DOI:
10.1002/jor.22928
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发表时间:
2015-11
影响因子:
2.8
通讯作者:
Shearn, Jason T.
Shearn, Jason T.
中科院分区:
医学3区
文献类型:
--
作者:
Lalley, Andrea L.;Dyment, Nathaniel A.;Kazemi, Namdar;Kenter, Keith;Gooch, Cynthia;Rowe, David W.;Butler, David L.;Shearn, Jason T.

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肌肉骨骼损伤极大地影响了美国人口,目前的临床方法无法恢复长期的天然组织结构和功能。组织工程是一种提倡改善肌腱愈合的策略;然而,该领域仍然需要建立评估组织工程结构有效性的生物学基准。研究卓越的愈合模型(例如 MRL/MpJ)提供了首先表征成功愈合的特征,然后将实验结果应用于组织工程疗法的机会。本研究旨在评估 MRL/MpJ 与野生型相比在中央髌腱损伤后的愈合反应。在损伤后 3、7 和 14 天评估基因表达和组织学,并在 2、5 和 8 周测量机械特性。天然髌腱的生物学和机械特性在品系之间没有差异。受伤后,MRL/MpJ 在 5 至 8 周内表现出机械性能增强;然而,菌株之间的早期肌腱表达模式没有差异。此外,细胞周期蛋白依赖性激酶抑制剂 p21 的表达在菌株之间没有差异,这表明可能有另一种机制正在驱动愈合反应。未来的研究将调查修复组织的胶原蛋白结构和排列,并表征完整的愈合转录组,以确定驱动 MRL/MpJ 反应的机制。
Musculoskeletal injuries greatly affect the U.S. population and current clinical approaches fail to restore long-term native tissue structure and function. Tissue engineering is a strategy advocated to improve tendon healing; however, the field still needs to establish biological benchmarks for assessing the effectiveness of tissue-engineered structures. Investigating superior healing models, such as the MRL/MpJ, offers the opportunity to first characterize successful healing and then apply experimental findings to tissue-engineered therapies. This study seeks to evaluate the MRL/MpJ’s healing response following a central patellar tendon injury compared to wildtype. Gene expression and histology were assessed at 3, 7, and 14 days following injury and mechanical properties were measured at 2, 5, and 8 weeks. Native patellar tendon biological and mechanical properties were not different between strains. Following injury, the MRL/MpJ displayed increased mechanical properties between 5 and 8 weeks; however, early tenogenic expression patterns were not different between the strains. Furthermore, expression of the cyclin-dependent kinase inhibitor, p21, was not different between strains, suggesting an alternative mechanism may be driving the healing response. Future studies will investigate collagen structure and alignment of the repair tissue and characterize the complete healing transcriptome to identify mechanisms driving the MRL/MpJ response.
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