Affiliations: [a] Department of Bioengineering, Northeastern University, Boston, MA, USA | [b] Department of Chemical Engineering, Northeastern University, Boston, MA, USA | [c] Department of Neuroscience, Albert Einstein College of Medicine, New York, NY, USA
Correspondence:
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Corresponding author: Eno E. Ebong, Ph.D., Department of Chemical Engineering, Northeastern University, 360 Huntington Avenue, 313 Snell Engineering Building, Boston, MA, 02115, USA. Tel.: +1 617 373 8744; Fax: +1 617 373 6696; E-mail: e.ebong@northeastern.edu
Abstract: BACKGROUND:The onset of many disease processes depends on the function of the endothelial cell (EC) glycocalyx (GCX) which acts as a flow-dependent barrier to cellular infiltration and molecular transport across the blood vessel wall. OBJECTIVE:This review aims to examine these processes with the potential end goal of implementing GCX repair to restore EC barrier function and slow the progression of disease. METHODS:Cell and mouse studies were employed to examine the state of EC GCX in healthy versus disruptive flow conditions. Correlations of observations of the GCX with a number of EC functions were sought with an emphasis on studies of trans-endothelial barrier integrity against vessel wall infiltration of cells and molecules from the circulation. To demonstrate the importance of GCX as a regulator of trans-endothelial infiltration, assays were performed using ECs with an intact GCX and compared to assays of ECs with an experimentally degraded GCX. Studies were also conducted of ECs in which a degraded GCX was repaired. RESULTS:In healthy flow conditions, the EC GCX was found to be thick and substantially covered the endothelial surface. GCX expression dropped significantly in complex flow conditions and coincided with a disease-like cellular and molecular accumulation in the endothelium or within the blood vessel wall. Therapeutic repair of the GCX abolished this accumulation. CONCLUSIONS:Regenerating the degraded GCX reverses EC barrier dysfunction and may attenuate the progression of vascular disease.
