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白细胞介素-1β可增加人生物人工肌腱的弹性。

Interleukin-1beta increases elasticity of human bioartificial tendons.

作者信息

Qi Jie, Chi Liqun, Maloney Melissa, Yang Xi, Bynum Donald, Banes Albert J

机构信息

Flexcell International Corp., Hillsborough, North Carolina, USA.

出版信息

Tissue Eng. 2006 Oct;12(10):2913-25. doi: 10.1089/ten.2006.12.2913.

DOI:10.1089/ten.2006.12.2913
PMID:17518659
Abstract

Stiffness is an important mechanical property of connective tissues, especially for tissues subjected to cyclic strain in vivo, such as tendons. Therefore, modulation of material properties of native or engineered tissues is an important consideration for tissue repair. Interleukin 1-beta (IL-1beta) is a cytokine most often associated in connective tissues with induction of matrix metalloproteinases and matrix destruction. However, IL-1beta may also be involved in constructive remodeling and confer a cell survival value to tenocytes. In this study, we investigated the effects of IL-1beta on the properties of human tenocyte-populated bioartificial tendons (BATs) fabricated in a novel three-dimensional (3D) culture system. IL-1beta treatment reduced the ultimate tensile strength and elastic modulus of BATs and increased the maximum strain. IL-1beta at low doses (1, 10 pM) upregulated elastin expression and at a high dose (100 pM) downregulated type I collagen expression. Matrix metalloproteinases, which are involved in matrix remodeling, were also upregulated by IL-1beta. The increased elasticity prevented BATs from rupture caused by applied strain. The results in this study suggest that IL-1beta may act as a defense/survival factor in response to applied mechanical loading. The balance between cell intrinsic strain and external matrix strain is important for maintaining the integrity of tendons.

摘要

硬度是结缔组织的一项重要力学特性,对于诸如肌腱等在体内承受循环应变的组织而言尤为如此。因此,调节天然组织或工程组织的材料特性是组织修复的一个重要考量因素。白细胞介素1β(IL-1β)是一种细胞因子,在结缔组织中通常与基质金属蛋白酶的诱导和基质破坏相关联。然而,IL-1β也可能参与建设性重塑,并赋予肌腱细胞存活价值。在本研究中,我们调查了IL-1β对在新型三维(3D)培养系统中构建的人肌腱细胞填充生物人工肌腱(BAT)特性的影响。IL-1β处理降低了BAT的极限拉伸强度和弹性模量,并增加了最大应变。低剂量(1、10 pM)的IL-1β上调了弹性蛋白表达,而高剂量(100 pM)则下调了I型胶原蛋白表达。参与基质重塑的基质金属蛋白酶也被IL-1β上调。弹性增加可防止BAT因施加的应变而破裂。本研究结果表明,IL-1β可能作为一种防御/存活因子来应对施加的机械负荷。细胞内在应变与外部基质应变之间的平衡对于维持肌腱的完整性很重要。

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