| First Author | Norman KE | Year | 2000 |
| Journal | Blood | Volume | 96 |
| Issue | 10 | Pages | 3585-91 |
| PubMed ID | 11071658 | Mgi Jnum | J:65810 |
| Mgi Id | MGI:1927323 | Doi | 10.1182/blood.v96.10.3585.h8003585_3585_3591 |
| Citation | Norman KE, et al. (2000) P-selectin glycoprotein ligand-1 supports rolling on E- and P-selectin in vivo. Blood 96(10):3585-91 |
| abstractText | Selectin-dependent rolling is the earliest observable event in the recruitment of leukocytes to inflamed tissues. Several glycoproteins decorated with sialic acid, fucose, and/or sulfate have been shown to bind the selectins. The best-characterized selectin ligand is P-selectin glycoprotein-1 (PSGL-1) that supports P-selectin- dependent rolling in vitro and in vivo. In vitro studies have suggested that PSGL-1 may also be a ligand for E- and L-selectins. To study the in vivo function of PSGL-1, without the influence of other leukocyte proteins, the authors observed the interaction of PSGL-1-coated microspheres in mouse venules stimulated to express P- and/or E-selectin. Microspheres coated with functional recombinant PSGL-1 rolled in surgically stimulated and tumor necrosis factor alpha (TNFalpha)-stimulated mouse venules. P-selectin deficiency or inhibition abolished microsphere rolling in surgically and TNFalpha-stimulated venules, whereas E-selectin deficiency or inhibition increased microsphere rolling velocity in TNFalpha-stimulated venules. The results suggest that P-selectin-PSGL-1 interaction alone is sufficient to mediate rolling in vivo and that E-selectin-PSGL-1 interaction supports slow rolling. (Blood. 2000;96:3585-3591) |
