TY  - JOUR
AB  - High dietary salt (NaCl) is a known risk factor for cardiovascular pathologies and inflammation. High plasma Na+ concentrations (high Na+) have been shown to stiffen the endothelial cortex and decrease nitric oxide (NO) release, a hallmark of endothelial dysfunction. Here we report that chronic high Na+ damages the endothelial glycocalyx (eGC), induces release of inflammatory cytokines from the endothelium and promotes monocyte adhesion. Single cell force spectroscopy reveals that high Na+ enhances vascular adhesion protein-1 (VCAM-1)-dependent adhesion forces between monocytes and endothelial surface, giving rise to increased numbers of adherent monocytes on the endothelial surface. Mineralocorticoid receptor antagonism with spironolactone prevents high Na+-induced eGC deterioration, decreases monocyte-endothelium interactions, and restores endothelial function, indicated by increased release of NO. Whereas high Na+ decreases NO release, it induces endothelial release of the pro-inflammatory cytokines IL-1ß and TNFα. However, in contrast to chronic salt load (hours), in vivo and in vitro, an acute salt challenge (minutes) does not impair eGC function. This study identifies the eGC as important mediator of inflammatory processes and might further explain how dietary salt contributes to endothelialitis and cardiovascular pathologies by linking endothelial nanomechanics with vascular inflammation.
AU  - Schierke, Florian Alexander
AU  - Wyrwoll, Margot Julia
AU  - Wisdorf, Martin
AU  - Niedzielski, Leon
AU  - Maase, Martina
AU  - Ruck, Tobias
AU  - Meuth, Sven
AU  - Meuth, Sven G.
AU  - Kusche-Vihrog, Kristina
DA  - 2017-04-13
DO  - 10.1038/srep46476
LA  - eng
N1  - Scientific Reports 7 (2017) 46476, 1-11
N1  - Finanziert durch den Open-Access-Publikationsfonds 2017 der Westfälischen Wilhelms-Universität Münster (WWU Münster).
PY  - 2017-04-13
TI  - Nanomechanics of the endothelial glycocalyx contribute to Na+-induced vascular inflammation
UR  - https://nbn-resolving.org/urn:nbn:de:hbz:6-68179620671
Y2  - 2024-11-24T00:18:14
ER  -