Roles of mechanical force and CXCR1/CXCR2 in shear-stress-induced endothelial cell migration |
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Authors: | Ye Zeng Yang Shen Xian-Liang Huang Xiao-Jing Liu Xiao-Heng Liu |
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Institution: | (1) Laboratory of Cardiovascular Diseases, West China Hospital, Sichuan University, No.17 Renmin Nanlu 3 Duan, Chengdu, 610041, People’s Republic of China;(2) Institute of Biomedical Engineering, West China School of Preclinical and Forensic Medicine, Sichuan University, Chengdu, People’s Republic of China; |
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Abstract: | We previously demonstrated that CXCR1 and CXCR2 are novel mechanosensors mediating laminar shear-stress-induced endothelial
cell (EC) migration (Zeng et al. in Cytokine 53:42–51, 2011). In the present study, an analytical model was proposed to further analyze the underlying mechanisms, assuming the mechanical
force (MF) and mechanosensor-mediated biochemical reactions induce cell migration together. Shear stress can regulate both
mechanosensor-mediated migration in the flow direction (Ms–MFD) and mechanosensor-mediated migration toward a wound (Ms–MW). Next, the migration distance, the roles of MF-induced cell migration (MF–M), and the mobilization mechanisms of mechanosensors
were analyzed. The results demonstrated that MF–M plays an important role in 15.27 dyn/cm2 shear-stress-induced EC migration but is far weaker than Ms–MW at 5.56 dyn/cm2. Our findings also indicated that CXCR2 played a primary role, in synergy with CXCR1. The Ms–MFD was primarily mediated by the synergistic effect of CXCR1 and CXCR2. In Ms–MW, when shear stress was beyond a certain threshold, the synergistic effect of CXCR1 and CXCR2 was enhanced, and the effect
of CXCR1 was inhibited. Therefore, the retarding of EC migration and wound closure capacity under low shear flow was related
to the low magnitude of shear stress, which may contribute to atherogenesis and many other vascular diseases. |
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