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Rapid Whole-Mount High-Resolution Imaging of Small Animal Vasculature for Quantitative Studies
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Hemodynamic force triggers rapid NETosis within sterile thrombotic occlusions.

X Yu1, J Tan1, S L Diamond1

  • 11024 Vagelos Research Laboratory, Department of Chemical and Biomolecular Engineering, Institute for Medicine and Engineering, University of Pennsylvania, Philadelphia, PA, USA.

Journal of Thrombosis and Haemostasis : JTH
|November 21, 2017
PubMed
Summary

High shear stress from blood flow, specifically arterial conditions, triggers neutrophil extracellular traps (NETs) release during sterile thrombosis. These NETs are rapidly released when hemodynamic forces exceed thresholds, indicating a physical mechanism for NETosis.

Keywords:
extracellular trapshemodynamicshistoneneutrophilthrombosis

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Area of Science:

  • Hematology
  • Biophysics
  • Cardiovascular Research

Background:

  • Neutrophil extracellular traps (NETs) are crucial in host defense against pathogens, particularly during sepsis.
  • NETosis is also implicated in thrombotic events, including venous and arterial thrombosis, and disseminated intravascular coagulation.

Purpose of the Study:

  • To investigate the role of hemodynamic forces in triggering NETosis during sterile thrombosis.
  • To elucidate the specific conditions under which shear stress drives NET formation in microfluidic models.

Main Methods:

  • Utilized microfluidic systems to perfuse human whole blood over collagenous surfaces under varying shear rates (venous and arterial).
  • Monitored NET formation using Sytox Green imaging, analyzing NETs' composition and sensitivity to inhibitors.
  • Measured pressure gradients and calculated fluid shear stress across occlusions.

Main Results:

  • Arterial shear rates (1000 s⁻¹) significantly induced NETosis compared to venous shear rates (100 s⁻¹), even without thrombin.
  • A rapid shift from venous to arterial flow conditions triggered NETosis within minutes, with NET levels increasing substantially.
  • High pressure gradients (>70 mmHg/mm-clot) correlated with shear stress exceeding 150 dyne cm⁻², driving NET release.

Conclusions:

  • Elevated interstitial hemodynamic forces, particularly high shear stress in arterial flow, are sufficient to induce rapid NET release during sterile occlusive thrombosis.
  • This suggests a physical mechanism, independent of certain biochemical pathways, by which mechanical forces drive NETosis in thrombosis.