Release of tensile strain on engineered human tendon tissue disturbs cell adhesions, changes matrix architecture, and induces an inflammatory phenotype.
Release of tensile strain on engineered human tendon tissue disturbs cell adhesions, changes matrix architecture, and induces an inflammatory phenotype.
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DOI：
10.1371/journal.pone.0086078
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Kjaer M
中科院分区：
文献类型：
--
作者：
Bayer ML;Schjerling P;Herchenhan A;Zeltz C;Heinemeier KM;Christensen L;Krogsgaard M;Gullberg D;Kjaer M
肌腱细胞的机械负荷会导致机械传导信号通路、细胞-基质粘附和胶原蛋白合成的上调，但卸载是否会消除这些反应尚不清楚。我们研究了张力释放的反应，关于基质蛋白，促炎介质和肌腱表型特异性分子，在体外模型中，肌腱样组织是从人肌腱细胞工程。在肌腱结构的手术去张力后1、2、4和6天进行组织取样。当张力刺激被去除时，整合素型胶原受体表现出相反的反应，整合素亚基α 11 mRNA和蛋白表达明显下降，而α 2整合素mRNA和蛋白水平增加。此外，肌腱细胞分化的特异性标志物下降，正常的肌腱结构受到干扰，而促炎分子上调。细胞因子TGF-β 1的刺激对张力和去张力组织中的一些肌腱相关基因有不同的影响。这些发现表明机械负荷对肌腱中细胞和基质反应的重要作用，包括张力损失导致肌腱表型标记物减少，同时诱导促炎介质的表达。
Mechanical loading of tendon cells results in an upregulation of mechanotransduction signaling pathways, cell-matrix adhesion and collagen synthesis, but whether unloading removes these responses is unclear. We investigated the response to tension release, with regard to matrix proteins, pro-inflammatory mediators and tendon phenotypic specific molecules, in an in vitro model where tendon-like tissue was engineered from human tendon cells. Tissue sampling was performed 1, 2, 4 and 6 days after surgical de-tensioning of the tendon construct. When tensile stimulus was removed, integrin type collagen receptors showed a contrasting response with a clear drop in integrin subunit α11 mRNA and protein expression, and an increase in α2 integrin mRNA and protein levels. Further, specific markers for tendon cell differentiation declined and normal tendon architecture was disturbed, whereas pro-inflammatory molecules were upregulated. Stimulation with the cytokine TGF-β1 had distinct effects on some tendon-related genes in both tensioned and de-tensioned tissue. These findings indicate an important role of mechanical loading for cellular and matrix responses in tendon, including that loss of tension leads to a decrease in phenotypical markers for tendon, while expression of pro-inflammatory mediators is induced.
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影响因子：
2.4
作者：
Ansorge, Heather L.;Adams, Sheila;Soslowsky, Louis J.
通讯作者：
Soslowsky, Louis J.
影响因子：
4.8
作者：
Carracedo, Sergio;Lu, Ning;Gullberg, Donald
通讯作者：
Gullberg, Donald
DOI：
10.1097/00005768-200003000-00012
发表时间：
2000-03-01
期刊：
MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
影响因子：
--
作者：
Giddings, VL;Beaupré, GS;Carter, DR
通讯作者：
Carter, DR
影响因子：
56.9
作者：
Cukierman, E;Pankov, R;Yamada, KM
通讯作者：
Yamada, KM
影响因子：
3.6
作者：
Chang, J;Thunder, R;Lineaweaver, WC
通讯作者：
Lineaweaver, WC