The effects of fluid shear stress on proliferation and osteogenesis of human periodontal ligament cells

被引:32
作者
Zheng, Lisha [1 ]
Chen, Luoping [1 ]
Chen, Yuchao [1 ]
Gui, Jinpeng [1 ]
Li, Qing [3 ]
Huang, Yan [1 ]
Liu, Meili [1 ]
Jia, Xiaolin [1 ]
Song, Wei [1 ]
Ji, Jing [1 ]
Gong, Xianghui [1 ]
Shi, Ruoshi [4 ]
Fan, Yubo [1 ,2 ]
机构
[1] Beihang Univ, Key Lab Biomech & Mech, Minist Educ, Sch Biol Sci & Med Engn, Beijing 100191, Peoples R China
[2] Natl Res Ctr Rehabil Tech Aids, Beijing 100176, Peoples R China
[3] Peking Univ, Ctr Digital Dent, Sch & Hosp Stomatol, Natl Engn Lab Digital & Mat Technol Stomatol, Beijing 100081, Peoples R China
[4] Ontario Canc Inst, Univ Hlth Network, Princess Margaret Canc Ctr, 500 Sherbourne St, Toronto, ON M4X 1K9, Canada
基金
中国国家自然科学基金;
关键词
Human periodontal ligament cells; Proliferation; Migration; Osteogenesis; Shear stress; MESENCHYMAL STEM-CELLS; SIGNALING PATHWAYS; CYCLE ARREST; IN-VITRO; FIBER ALIGNMENT; GROWTH-FACTOR; MAP KINASE; TISSUE; FLOW; DIFFERENTIATION;
D O I
10.1016/j.jbiomech.2016.01.034
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
Shear stress is one of the main stress type produced by speech, mastication or tooth movement. The mechano-response of human periodontal ligament (PDL) cells by shear stress and the mechanism are largely unknown. In our study, we investigated the effects of fluid shear stress on proliferation, migration and osteogenic potential of human PDL cells. 6 dyn/cm(2) of fluid shear stress was produced in a parallel plate flow chamber. Our results demonstrated that fluid shear stress rearranged the orientation of human PDL cells. In addition, fluid shear stress inhibited human PDL cell proliferation and migration, but increased the osteogenic potential and expression of several growth factors and cytokines. Our study suggested that shear stress is involved in homeostasis regulation in human PDL cells. Inhibiting proliferation and migration potentially induce PDL cells to respond to mechanical stimuli in order to undergo osteogenic differentiation. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:572 / 579
页数:8
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