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rhAPC reduces the endothelial cell permeability via a decrease of contractile tensions induced by endothelial cells.

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This study shows lipopolysaccharide (LPS) increases human aortic endothelial cell (HAoEC) tension, a key factor in sepsis. Recombinant activated protein C (rhAPC) effectively reversed this harmful cellular tension.

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Area of Science:

  • Cellular mechanics
  • Endothelial cell biology
  • Sepsis research

Background:

  • Cellular contractile tension is vital for cell function and survival.
  • Gram-negative sepsis, triggered by lipopolysaccharide (LPS), increases endothelial cell permeability.
  • Understanding cellular mechanical responses is crucial for sepsis treatment.

Purpose of the Study:

  • To investigate the effect of LPS on human aortic endothelial cell (HAoEC) mechanical tension.
  • To determine if recombinant activated protein C (rhAPC) can reverse LPS-induced cellular tension.
  • To validate the CellDrum technology for quantifying cellular mechanical tension.

Main Methods:

  • Utilized CellDrum technology to measure pico-scale cellular mechanical tension.
  • Established an in-vitro sepsis model confirmed by IL-6 levels, ROS activation, and RhoA mRNA expression.
  • Used thrombin-induced contraction as a positive control for endothelial cell contraction.

Main Results:

  • LPS significantly increased HAoEC contractile tension, linked to actin stress fiber predominance.
  • This increased tension led to enhanced endothelial contractility and permeability.
  • rhAPC demonstrated a beneficial effect in reversing sepsis-induced cellular tension.

Conclusions:

  • CellDrum technology accurately quantifies cellular mechanical tension.
  • rhAPC shows therapeutic potential by mitigating sepsis-related cellular mechanical dysfunction.
  • The CellDrum technology is promising for high-throughput analysis of pathological cellular tension.