| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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.
This article has been cited by other articles:
|
|
 |
|
  P. Robert, K. Sengupta, P.-H. Puech, P. Bongrand, and L. Limozin Tuning the Formation and Rupture of Single Ligand-Receptor Bonds by Hyaluronan-Induced Repulsion Biophys. J., October 15, 2008; 95(8): 3999 - 4012. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. Tarbell and E. E. Ebong The Endothelial Glycocalyx: A Mechano-Sensor and -Transducer Sci. Signal., October 7, 2008; 1(40): pt8 - pt8. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Banz, R. Rieben, C. Zobrist, P. Meier, S. Shaw, J. Lanz, T. Carrel, and P. Berdat Addition of dextran sulfate to blood cardioplegia attenuates reperfusion injury in a porcine model of cardiopulmonary bypass Eur. J. Cardiothorac. Surg., September 1, 2008; 34(3): 653 - 660. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. W. G. E. VanTeeffelen, A. A. Constantinescu, J. Brands, J. A. E. Spaan, and H. Vink Bradykinin- and sodium nitroprusside-induced increases in capillary tube haematocrit in mouse cremaster muscle are associated with impaired glycocalyx barrier properties J. Physiol., July 1, 2008; 586(13): 3207 - 3218. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. Haraldsson, J. Nystrom, and W. M. Deen Properties of the Glomerular Barrier and Mechanisms of Proteinuria Physiol Rev, April 1, 2008; 88(2): 451 - 487. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Banz, O. M. Hess, S. C. Robson, E. Csizmadia, D. Mettler, P. Meier, A. Haeberli, S. Shaw, R. A. Smith, and R. Rieben Attenuation of myocardial reperfusion injury in pigs by Mirococept, a membrane-targeted complement inhibitor derived from human CR1 Cardiovasc Res, December 1, 2007; 76(3): 482 - 493. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. W.G.E. VanTeeffelen, J. Brands, C. Jansen, J. A.E. Spaan, and H. Vink Heparin Impairs Glycocalyx Barrier Properties and Attenuates Shear Dependent Vasodilation in Mice Hypertension, July 1, 2007; 50(1): 261 - 267. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Bertuglia, F. M. Veronese, and G. Pasut Polyethylene glycol and a novel developed polyethylene glycol-nitric oxide normalize arteriolar response and oxidative stress in ischemia-reperfusion Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1536 - H1544. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. J. Bergan, G. W. Schmid-Schonbein, P. D. C. Smith, A. N. Nicolaides, M. R. Boisseau, and B. Eklof Chronic Venous Disease N. Engl. J. Med., August 3, 2006; 355(5): 488 - 498. [Full Text] [PDF]
|
|
|
|
|
|
I. Rubio-Gayosso, S. H. Platts, and B. R. Duling Reactive oxygen species mediate modification of glycocalyx during ischemia-reperfusion injury Am J Physiol Heart Circ Physiol, June 1, 2006; 290(6): H2247 - H2256. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Mehta and A. B. Malik Signaling Mechanisms Regulating Endothelial Permeability Physiol Rev, January 1, 2006; 86(1): 279 - 367. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Banz, O. M. Hess, S. C. Robson, D. Mettler, P. Meier, A. Haeberli, E. Csizmadia, E. Y. Korchagina, N. V. Bovin, and R. Rieben Locally targeted cytoprotection with dextran sulfate attenuates experimental porcine myocardial ischaemia/reperfusion injury Eur. Heart J., November 1, 2005; 26(21): 2334 - 2343. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Bruegger, M. Jacob, M. Rehm, M. Loetsch, U. Welsch, P. Conzen, and B. F. Becker Atrial natriuretic peptide induces shedding of endothelial glycocalyx in coronary vascular bed of guinea pig hearts Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H1993 - H1999. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Solic, J. Wilson, S. J. Wilson, and J. K. Shute Endothelial Activation and Increased Heparan Sulfate Expression in Cystic Fibrosis Am. J. Respir. Crit. Care Med., October 1, 2005; 172(7): 892 - 898. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
