PECAM-1 (Platelet-Endothelial Cell Adhesion Molecule-1, CD31) is critical in passage through the junction in cytokine-activated transmigration. Anti-PECAM-1 antibodies reduce monocyte transmigration through resting endothelium, and both monocyte and neutrophil transmigration through cytokine activated endothelium by 70-90% (Muller, 1995; Muller et al 1993). Binding of leukocytes to endothelium is not affected. The effects are seen if endothelial cells or leukocytes or both are treated with antibodies, and inhibition lasts at least 48 hours (Bogen et al 1994; Muller, 1995). The efficacy of PECAM-1 antibodies in vivo has been confirmed in other inflammatory models (Vaporciyan et al 1993; Muller, 1995). Monoclonal antibodies mapped to domain 1-2 inhibit transmigration, but other monoclonal antibodies are not inhibitory (Liao et al 1995). Although v3 integrin can be a ligand for PECAM-1 (Piali et al 1995), and monocytes lacking 3-integrin transmigrate poorly, this appears to be due to modulation of CD11a/CD18 rather than by an interaction with PECAM-1. Unlike many other endothelial cell adhesion molecules expression is not significantly upregulated by activation with TNF or IFN-g in usual doses (Romer et al 1995). Furthermore, PECAM-1 does not appear to be redistributed during cytokine or chemotactic transmigration (Allport et al. 1997).

In contrast to cytokine-activated transmigration, PECAM-1 seems to have little role in chemotactic transmigration. PECAM-1 antibodies do not decrease chemotactic transmigration in vivo (Wakelin et al 1996), nor do they decrease transmigration triggered by thrombin (Scalia et al 1998). In addition, there is often a significant residual transmigration (~10-30%) after PECAM-1 inhibition which suggests that other mechanisms may operate in passage through the junction in cytokine-activated transmigration. These observations suggest that the mechanisms operating in cytokine-activated and chemotactic transmigration overlap to only a small degree. The mechanism of PECAM-1 independent transmigration is unknown. Neutrophils and monocytes from CD11a knock out mice do not require PECAM-1 for transmigration (Andrew et al 1998), suggesting that CD11a and PECAM-1 somehow operate in a similar pathway of migration. However, PECAM-1 knockout mice show no clear evidence of a transmigration defect.

View various information about this molecule at the National Center for Biotechnology Information.


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