Differential arrest and adhesion of tumor cells and microbeads in the microvasculature
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  • 作者:Peng Guo (1)
    Bin Cai (1)
    Ming Lei (2)
    Yang Liu (2)
    Bingmei M. Fu (1)
  • 关键词:Mechanical trapping ; Cell deformability ; Hemodynamic factors ; Vorticity ; Shear rate ; Rat mesenteric microvasculature
  • 刊名:Biomechanics and Modeling in Mechanobiology
  • 出版年:2014
  • 出版时间:June 2014
  • 年:2014
  • 卷:13
  • 期:3
  • 页码:537-550
  • 全文大小:
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  • 作者单位:Peng Guo (1)
    Bin Cai (1)
    Ming Lei (2)
    Yang Liu (2)
    Bingmei M. Fu (1)

    1. Department of Biomedical Engineering, The City College of the City University of New York, 160 Convent Avenue, New York, NY, 10031, USA
    2. Department of Mechanical Engineering, The Hong Kong Polytechnic University, Kowloon Hong Kong, China
  • ISSN:1617-7940
文摘
To investigate the mechanical mechanisms behind tumor cell arrest in the microvasculature, we injected fluorescently labeled human breast carcinoma cells or similarly sized rigid beads into the systemic circulation of a rat. Their arrest patterns in the microvasculature of mesentery were recorded and quantified. We found that 93?% of rigid beads were arrested either at arteriole–capillary intersections or in capillaries. Only 3?% were at the capillary–postcapillary venule intersections and in postcapillary venules. In contrast, most of the flexible tumor cells were either entrapped in capillaries or arrested at capillary or postcapillary venule–postcapillary venule intersections and in postcapillary venules. Only 12?% of tumor cells were arrested at the arteriole–capillary intersections. The differential arrest and adhesion of tumor cells and microbeads in the microvasculature was confirmed by a \(\chi ^{2}\) test ( \(p<0.001\) ). These results demonstrate that mechanical trapping was responsible for almost all the arrest of beads and half the arrest of tumor cells. Based on the measured geometry and blood flow velocities at the intersections, we also performed a numerical simulation using commercial software (ANSYS CFX 12.01) to depict the detailed distribution profiles of the velocity, shear rate, and vorticity at the intersections where tumor cells preferred to arrest and adhere. Simulation results reveal the presence of localized vorticity and shear rate regions at the turning points of the microvessel intersections, implying that hemodynamic factors play an important role in tumor cell arrest in the microcirculation. Our study helps elucidate long-debated issues related to the dominant factors in early-stage tumor hematogenous metastasis.

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