The endothelial glycocalyx mediates shear-induced changes in hydraulic conductivity.
Recent in vitro and in vivo studies have reported fluid shear stress-induced increases in endothelial layer hydraulic conductivity (L(p)) that are mediated by an increased production of nitric oxide (NO). Other recent studies have shown that NO induction by shear stress is mediated by the glycocalyx that decorates the surface of endothelial cells. Here we find that a selective depletion of the major components of the glycocalyx with enzymes can block the shear stress-induced response of L(p). Heparinase and hyaluronidase block shear-induced increases in L(p), which is consistent with their effects on NO production. But chondroitinase, which does not suppress shear-induced NO production, also inhibits shear-induced L(p). A further surprise is that treatment with the general proteolytic enzyme pronase does not suppress the shear L(p) response. We also find that heparinase does not alter baseline L(p) significantly, whereas chondroitinase, hyaluronidase, and pronase increase it significantly.
Lopez-Quintero
Sandra V
SV
Dept. of Biomedical Engineering, The City College of the City Univ. of New York, Steinman Hall, Rm. T403, 140th St. and Convent Ave., New York, NY 10031, USA.
Amaya
Ronny
R
Pahakis
Manolis
M
Tarbell
John M
JM
D000818:Animals; D002417:Cattle; D002478:Cells, Cultured; D002810:Chondroitinases and Chondroitin Lyases / Q000378:metabolism; D042783:Endothelial Cells / Q000378:metabolism*; D019276:Glycocalyx / Q000378:metabolism*; D019763:Heparin Lyase / Q000378:metabolism; D006821:Hyaluronoglucosaminidase / Q000378:metabolism; D040542:Mechanotransduction, Cellular; D009569:Nitric Oxide / Q000378:metabolism*; D011312:Pressure; D011402:Pronase / Q000378:metabolism; D013314:Stress, Mechanical; D013997:Time Factors; D014867:Water / Q000378:metabolism
D014867:Water; D009569:Nitric Oxide; D006821:Hyaluronoglucosaminidase; D011402:Pronase; D002810:Chondroitinases and Chondroitin Lyases; D019763:Heparin Lyase