Severe impairment of leukocyte rolling in venules of core 2 glucosaminyltransferase-deficient mice

Blood. 2001 Jun 15;97(12):3812-9. doi: 10.1182/blood.v97.12.3812.

Abstract

Leukocyte capture and rolling are mediated by selectins expressed on leukocytes (L-selectin) and the vascular endothelium (P- and E-selectin). To investigate the role of core 2 beta1-6-N-glucosaminyltransferase (C2GlcNAcT-I) for synthesis of functional selectin ligands in vivo, leukocyte rolling flux and velocity were studied in venules of untreated and tumor necrosis factor-alpha (TNFalpha)-pretreated autoperfused cremaster muscles of C2GlcNAcT-I-deficient (core 2(-/-)) and littermate control mice. In untreated core 2(-/-) mice, leukocyte rolling was dramatically reduced with markedly increased rolling velocities (81 +/- 4 microm/s vs 44 +/- 3 microm/s). The reduced rolling in core 2(-/-) mice was due mainly to severely impaired binding of P-selectin to P-selectin glycoprotein ligand-1 (PSGL-1). Some rolling remained after blocking PSGL-1 in controls but not in core 2(-/-) mice. In TNFalpha-pretreated mice, rolling was markedly reduced in core 2(-/-) mice owing to impaired P-selectin- and E-selectin-mediated rolling. Rolling velocities in core 2(-/-) mice treated with an E-selectin-blocking monoclonal antibody (59 +/- 4 microm/s) were significantly higher than in controls (14 +/- 1 microm/s), which provides further evidence for the severe impairment in P-selectin-mediated rolling. In conclusion, P-selectin ligands including PSGL-1 are largely C2GlcNAcT-I dependent. In addition, E-selectin-mediated rolling in vivo is partially dependent on the targeted C2GlcNAcT-I. (Blood. 2001;97:3812-3819)

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Bone Marrow Cells / chemistry
  • Cell Adhesion / drug effects*
  • Cell Movement / drug effects
  • Disease Models, Animal
  • E-Selectin / drug effects
  • E-Selectin / metabolism
  • Endothelium, Vascular / metabolism
  • Endothelium, Vascular / pathology
  • Inflammation / chemically induced
  • Inflammation / pathology
  • Ligands
  • Membrane Glycoproteins / drug effects
  • Membrane Glycoproteins / metabolism
  • Mice
  • Mice, Knockout
  • N-Acetylglucosaminyltransferases / deficiency
  • N-Acetylglucosaminyltransferases / pharmacology*
  • Neutrophils / chemistry
  • P-Selectin / drug effects
  • P-Selectin / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology
  • Venules / enzymology*

Substances

  • E-Selectin
  • Ligands
  • Membrane Glycoproteins
  • P-Selectin
  • P-selectin ligand protein
  • Tumor Necrosis Factor-alpha
  • N-Acetylglucosaminyltransferases
  • beta-1,3-galactosyl-O-glycosyl-glycoprotein beta-1,6-acetylglucosaminyl transferase