The endothelial glycocalyx acts as a protective barrier in the context of bradykinin-mediated angioedema

Introduction Hereditary angioedema is a rare genetic disorder characterized by recurrent attacks of swelling. Edema of the upper respiratory tract can be fatal. The disease centers on bradykinin, which causes disruption of the endothelial barrier. This in turn is significantly established by the glycocalyx, a thin carbohydrate layer on the apical endothelial side. However, the exact role of this structure in the context of angioedema is still unknown.

Materials and methods Human umbilical vein endothelial cells were evaluated for barrier function by measuring electrical resistance, permeability, and water flux by D2O dilution method. The glycocalyx was studied by Wheat germ agglutinin assay and electron microscopy. To study its influence in more detail, it was degraded enzymatically. Changes in the expression of structures of the glycocalyx were detected by semi-quantitative RT-PCR.

Results Degradation of the glycocalyx resulted in increased endothelial permeability and, consequently, increased transendothelial water flow. Bradykinin, in turn, decreased endothelial barrier function via its B2 receptor. Previous degradation of the glycocalyx further significantly enhanced this effect.

Conclusion Our results demonstrated for the first time that damage to the glycocalyx leads to increased water permeability of the endothelium. Furthermore, we could show that the glycocalyx is a protective structure against bradykinin-mediated barrier disruption. This opens up new possibilities in the diagnosis and possibly prophylaxis of angioedema.

Publication History

Article published online:
12 May 2023