Study: In Vitro: 3 papers
Peer-reviewed work on the endothelial glycocalyx, microvascular health and the ingredients in our formulas, newest first. Abstracts are indexed here and every paper links to the journal.
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Published paper
Rhamnan sulfate enhances the endothelial glycocalyx and decreases the LDL permeability of human coronary artery endothelial cells in vitro
Human coronary artery endothelial cell monolayers were treated for 24 hours with two isoforms of rhamnan sulfate (a sulfated polysaccharide) and then tested for how easily LDL cholesterol crossed the cell layer. Both isoforms cut LDL permeability about 5-fold and prevented the permeability rise caused by chemically induced apoptosis, while immunostaining showed greater heparan sulfate coverage, a key glycocalyx component. The authors propose that a thicker glycocalyx adds resistance to the 'leaky junction' route that LDL uses to cross the endothelium.
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Published paper
A Dietary Supplement Containing Fucoidan Preserves Endothelial Glycocalyx through ERK/MAPK Signaling and Protects against Damage Induced by CKD Serum
Researchers tested whether a commercial dietary supplement containing fucoidan, glucosamine sulfate, hyaluronan and antioxidants could protect the endothelial glycocalyx in laboratory models. Using atomic force microscopy on living endothelial cells, the supplement and fucoidan alone increased glycocalyx thickness, prevented heparinase-induced degradation, and reversed thinning caused by pooled serum from hemodialysis patients; effects depended on ERK/MAPK (and to a lesser extent PI3K) signaling and Golgi-dependent vesicular transport. In mice fed the supplement for two weeks, sidestream dark-field imaging of cremaster microvessels showed a reduced perfused boundary region, consistent with a thicker glycocalyx.
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Published paper
Tie2 Activation Promotes Protection and Reconstitution of the Endothelial Glycocalyx in Human Sepsis
Researchers measured the perfused boundary region (PBR), an inverse marker of endothelial glycocalyx thickness, in sublingual microvessels of septic patients and nonseptic controls, and found thicker PBR (thinner glycocalyx) in sepsis that correlated with serum angiopoietin-2 levels. Serum from septic patients thinned the glycocalyx of cultured human endothelial cells, an effect abolished by blocking angiopoietin-2 or activating the Tie2 receptor. Mechanistically, damage required heparan sulfate loss via heparanase, which Tie2 activation suppressed; Tie2 activation after injury also accelerated glycocalyx recovery.
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