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Shear stress affects migration behavior of polymorphonuclear cells arrested on endothelium

J Kitayama1, A Hidemura, H Saito

  • 1Department of Surgery, The Surgical Center, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo, 113, Japan.

Cellular Immunology
|August 1, 2000
PubMed

Insights

Shear stress accelerates polymorphonuclear cell (PMN) transmigration across endothelial cells. Beta-1 integrins are crucial for PMN binding to the subendothelial matrix during leukocyte extravasation.

Area of Science:

  • Cellular Biology
  • Immunology
  • Biophysics

Background:

  • Leukocyte extravasation is a critical process in inflammation.
  • Endothelial cells form a barrier that polymorphonuclear cells (PMNs) must traverse.
  • Understanding the dynamics of PMN transmigration under flow is essential.

Purpose of the Study:

  • To investigate the effect of shear flow on PMN transmigration across TNF-alpha-stimulated endothelial cells.
  • To identify the molecular mechanisms, particularly integrin involvement, in PMN transmigration.
  • To elucidate the role of the subendothelial extracellular matrix in PMN migration.

Main Methods:

  • Time-lapse videotaping to monitor PMN transmigration across human umbilical vein endothelial cell (HUVEC) monolayers under shear flow.
  • Inhibition studies using anti-integrin monoclonal antibodies (mAbs) and RGD peptide.
  • HUVEC culture on fibronectin or laminin to assess matrix interactions.

Main Results:

  • Shear flow significantly accelerated PMN transmigration compared to static conditions.
  • Anti-beta1 integrin mAb (4B4) and RGD peptide were potent inhibitors of transmigration.
  • Binding to fibronectin and laminin via alpha5 and alpha6 integrins, respectively, was also shown to be important.

Conclusions:

  • Shear stress dynamically influences PMN migration behavior on the endothelium.
  • Beta-1 integrin-mediated binding to the subendothelial extracellular matrix is a key step in leukocyte extravasation.
  • Targeting beta-1 integrins may offer therapeutic strategies for inflammatory diseases.

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