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Multimodal Profiling Reveals Distinct Endothelial Activation Pathways Regulated by Flow and Heparan Sulfate.

Ian C Harding1, Nicholas R O'Hare2, Ira M Herman3,4,5

  • 1Department of Bioengineering, Northeastern University, Boston, MA USA.

Cellular and Molecular Bioengineering
|March 30, 2026
PubMed
Summary

Degradation of heparan sulfate (HS) in endothelial cells promotes inflammation and dysfunction, contributing to atherosclerosis. Intact HS protects against flow-dependent inflammation but does not affect reactive oxygen species (ROS) production.

Keywords:
Endothelial glycocalyxEndothelial inflammationMechanotransductionRNA sequencingReactive oxygen species

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Area of Science:

  • Cardiovascular Research
  • Cell Biology
  • Biomedical Engineering

Background:

  • Atherosclerotic cardiovascular disease stems from endothelial dysfunction, marked by inflammation and increased reactive oxygen species (ROS).
  • Adverse mechanical conditions like stagnant flow contribute to endothelial dysfunction, a precursor to atherosclerosis.
  • The endothelial glycocalyx, rich in heparan sulfate (HS), plays a crucial role in maintaining endothelial health.

Purpose of the Study:

  • To investigate how heparan sulfate (HS) degradation influences endothelial cell phenotype under varying flow conditions.
  • To determine the role of HS in the transition from a functional to a dysfunctional endothelial state.
  • To understand the link between HS, endothelial inflammation, and oxidative stress in the context of atherosclerosis.

Main Methods:

  • Human aortic endothelial cells were subjected to physiological shear stress (14 dynes/cm²) and static conditions (0 dynes/cm²).
  • Enzymatic degradation of HS was induced using heparinase III to simulate glycocalyx damage.
  • Endothelial cell phenotype was analyzed using techniques including fluorescent labeling, confocal microscopy, Western blotting, and RNA sequencing.

Main Results:

  • Cells under 14 dynes/cm² shear stress without HS degradation showed low inflammatory gene expression and minimal ROS production.
  • Heparinase III-induced HS degradation under flow conditions triggered an inflammatory phenotype, similar to static conditions.
  • ROS levels were not significantly affected by HS degradation, suggesting HS primarily modulates inflammation.

Conclusions:

  • Intact heparan sulfate (HS) is critical for mitigating endothelial inflammation associated with flow-dependent atherosclerosis.
  • HS degradation promotes a pro-inflammatory endothelial phenotype, contributing to the development of atherosclerotic cardiovascular disease.
  • Targeting HS represents a potential therapeutic strategy for atherosclerotic cardiovascular disease, distinct from interventions focused on ROS.