C-reactive protein impairs the endothelial glycocalyx resulting in endothelial dysfunction

Area of Science:

• Cardiovascular Biology
• Inflammation Research
• Endothelial Function

Background:

• Atherosclerosis involves inflammation and endothelial dysfunction.
• C-reactive protein (CRP) is a key inflammatory marker linked to cardiovascular risk and endothelial dysfunction.
• The endothelial glycocalyx is crucial for protecting the endothelium.

Purpose of the Study:

• To investigate the impact of C-reactive protein (CRP) on the endothelial glycocalyx.
• To determine if CRP affects glycocalyx thickness and composition.

Main Methods:

• Human aortic endothelial cells (HAECs) were treated with varying concentrations of CRP in vitro.
• CRP was administered to rats in vivo, with controls used for both experiments.
• Glycocalyx thickness was assessed using transmission electron microscopy.
• Hyaluronan (HA) release and heparan sulfate (HS) expression were quantified.

Main Results:

• CRP significantly increased HA release in both cell cultures and animal models.
• A dose-dependent decrease in endothelial glycocalyx thickness was observed with CRP exposure.
• CRP treatment led to a significant reduction in HS expression.
• Increased HA release correlated with heightened monocyte-endothelial cell adhesion and inflammatory markers, and reduced nitric oxide synthase activity.

Conclusions:

• C-reactive protein (CRP) negatively impacts endothelial glycocalyx integrity and function.
• Impairment of the glycocalyx by CRP contributes to endothelial dysfunction, a critical step in atherosclerosis development.