L-selectin-dependent leukocyte adhesion to microvascular but not to macrovascular endothelial cells of the human coronary system
- A. Zakrzewicz(corresponding author),
- M. Gräfe,
- D. Terbeek,
- M. Bongrazio,
- W. Auch-Schwelk,
- B. Walzog
- Free University of Berlin,
- Deutsches Herz-Zentrum Berlin,
- University of Virginia,
- ,
- ,
Open access
Abstract
To characterize L-selectin-dependent cell adhesion to human vascular endothelium, human cardiac microvascular endothelial cells (HCMEC) and human coronary endothelial cells (HCEC) were isolated from explanted human hearts. The adhesion behavior of human (NALM-6) and mouse (300.19) pre-B cells transfected with cDNA encoding for human L-selectin was compared with that of the respective nontransfected cells in a flow chamber in vitro. More than 80% of the adhesion to tumor necrosis factor-α (TNF-α)stimulated HCMEC at shear stresses >2 dyne/cm2 was L-selectin dependent and could be equally well blocked by an anti-L-selectin antibody or a L-selectin-IgG-chimera. No L- selectin dependent adhesion to HCEC could be shown. The L-selectin dependent adhesion to HCMEC was insensitive to neuraminidase, but greatly inhibited by addition of NaCIO3, which inhibits posttranslational sulfation and remained elevated for at least 24 hours of stimulation. E-selectin dependent adhesion of HL60 cells to HCMEC was blocked by neuraminidase, but not by NaCIO3 and returned to control levels within 18 hours of HCMEC stimulation. It is concluded that microvascular, but not macrovascular endothelial cells express TNF-α-inducible sulfated ligand(s) for L-selectin, which differ from known L-selectin ligands, because sialylation is not required. The prolonged time course of L-selectin dependent adhesion suggests a role in sustained leukocyte recruitment into inflammatory sites in vivo.
Publication Information
Output type
Original language
English (US)Pages from-to (Number of pages)
Pages 3228-3235 (8 pages)Journal (Volume, Issue Number)
Blood (Volume 89, Issue 9)Publication milestones
- Published - 05/01/1997
Publication status
ISSN
0006-4971Publication IDs
- Scopus: 1842413690
- PubMed: 9129027
