Friction-Induced Apoptosis

Friction-Induced Apoptosis
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摩擦诱导的细胞凋亡

DOI:
10.1007/s11249-019-1197-0
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发表时间:
2019
期刊:
影响因子:
3.2
通讯作者:
A. Pitenis
A. Pitenis
中科院分区:
工程技术2区
文献类型:
--
作者:
Samuel M. Hart;George D. Degen;J. Urueña;P. Levings;W. Sawyer;A. Pitenis

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上皮细胞在体内形成摩擦学滑动界面,通常是组织和器官的衬里,并产生高含水量的粘蛋白凝胶,从而保护底层细胞、组织、膜和器官免受损伤。摩擦和由此产生的直接接触剪切应力已被证明可诱导促炎细胞因子的产生,并上调与程序性细胞死亡(凋亡)相关的基因。利用永生化角膜上皮细胞单层、原位荧光显微镜和带水凝胶探针的微摩擦仪,在急性和慢性条件下进行了一系列实验,以探讨这些细胞凋亡的发生条件和进展。结果表明,细胞凋亡发生在低于100 Pa的生理剪切应力附近。有趣的是,在没有滑动的情况下,即使在接近3kpa的压力下,直接接触压力也不会引发细胞凋亡。
Epithelial cells form tribological sliding interfaces through the body, often lining tissues and organs, and produce high-water-content mucin gels, thereby protecting underlying cells, tissues, membranes, and organs from damage. Friction and the resulting direct contact shear stresses have been shown to induce the production of pro-inflammatory cytokines and upregulate genes associated with programmed cell death (apoptosis). Using monolayers of immortalized corneal epithelial cells, in situ fluorescence microscopy, and a microtribometer with aqueous gel probes, a series of experiments were performed under acute and chronic conditions to explore onset conditions and progression of apoptosis of these cells. The results reveal that the initiation of apoptosis occurs near physiological shear stresses below 100 Pa. Interesting, the direct contact pressures in the absence of sliding did not initiate apoptosis even at pressures approaching 3 kPa.
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