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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Arterioscler+Thromb+Vasc+Biol
2018 ; 38
(7
): 1427-1439
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Endothelial Glycocalyx as a Shield Against Diabetic Vascular Complications:
Involvement of Hyaluronan and Hyaluronidases
#MMPMID29880486
Dogné S
; Flamion B
; Caron N
Arterioscler Thromb Vasc Biol
2018[Jul]; 38
(7
): 1427-1439
PMID29880486
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The endothelial glycocalyx (EG), which covers the apical surface of the
endothelial cells and floats into the lumen of the vessels, is a key player in
vascular integrity and cardiovascular homeostasis. The EG is composed of PGs
(proteoglycans), glycoproteins, glycolipids, and glycosaminoglycans, in
particular hyaluronan (HA). HA seems to be implicated in most of the functions
described for EG such as creating a space between blood and the endothelium,
controlling vessel permeability, restricting leukocyte and platelet adhesion, and
allowing an appropriate endothelial response to flow variation through
mechanosensing. The amount of HA in the EG may be regulated by HYAL
(hyaluronidase) 1, the most active somatic hyaluronidase. HYAL1 seems enriched in
endothelial cells through endocytosis from the bloodstream. The role of the other
main somatic hyaluronidase, HYAL2, in the EG is uncertain. Damage to the EG,
accompanied by shedding of one or more of its components, is an early sign of
various pathologies including diabetes mellitus. Shedding increases the blood or
plasma concentration of several EG components, such as HA, heparan sulfate, and
syndecan. The plasma levels of these molecules can then be used as sensitive
markers of EG degradation. This has been shown in type 1 and type 2 diabetic
patients. Recent experimental studies suggest that preserving the size and amount
of EG HA in the face of diabetic insults could be a useful novel therapeutic
strategy to slow diabetic complications. One way to achieve this goal, as
suggested by a murine model of HYAL1 deficiency, may be to inhibit the function
of HYAL1. The same approach may succeed in other pathological situations
involving endothelial dysfunction and EG damage.
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