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1 Department of Bioengineering, The Pennsylvania State University, University Park, PA, USA
* To whom correspondence should be addressed. E-mail: hhlbio{at}engr.psu.edu.
Alterations in composition of the glycocalyx of venular endothelium in post-capillary venules (rat mesentery) were explored in models of inflammation and ischemia/reperfusion injury. Lectins were covalently linked to fluorescently labeled microspheres (0.1 m diameter) or directly labeled with fluorescein-isothiocyanate (FITC). Adhesion of lectins specific for glucose and galactose residues of glycosaminoglycans (GAGs) and other components of the endothelial glycocalyx decreased dramatically following superfusion of the mesentery with the chemoattractant f-met-leu-phe (fMLP), and during reperfusion following a 60 min ischemic period. These reductions were significantly attenuated by superfusion with pertussis toxin (PTX), thus suggesting that shedding of glycocalyx was mediated by G-Proteins. Adhesion of microspheres linked with antibody for syndecan-1, a major proteoglycan to which the GAGs are bound, revealed increased labeling as GAGs were lost and permitted greater numbers of spheres to adhere to the protein core, which was not shed. Induction of ischemia by occluding proximal microvessels for 60 min, resulted in a 40% increase in galactosaminoglycans and a 15% increase in glucosaminoglycans on the endothelium, that was not inhibited by PTX. Reperfusion of the vessels led to a rapid loss of GAGs that was inhibited by pre-treatment with PTX, with 40% of the galactosaminoglycans and 25% of the glucosaminoglycans accumulated being removed by G-protein mediated shedding, and the remainder being freely convected away by fluid shear. It is concluded that the composition of the glycocalyx results from a balance of the rate of biosynthesis of GAGs by the EC, and their shedding which may be mediated by intracellular and/or membrane bound proteases or lyases released or activated by G-protein signaling.
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