Abstract
Filopodia are an important feature of actively motile cells, probing the pericellular environment for chemotactic factors and other molecular cues that enable and direct the movement of the cell. They also act as points of attachment to the extracellular matrix for the cell, generating tension that may act to pull the cell forward and/or stabilize the cell as it moves. Endothelial cell motility is a critical aspect of angiogenesis, but only a limited number of molecules have been identified as specific regulators of endothelial cell filopodia. Recent reports, however, provide evidence for the involvement of PECAM-1, an endothelial cell adhesion and signaling molecule, in the formation of endothelial cell filopodia. This commentary will focus on these studies and their suggestion that at least two PECAM-1-regulated pathways are involved in the processes that enable filopodial protrusions by endothelial cells. Developing a more complete understanding of the role of PECAM-1 in mediating various endothelial cell activities, such as the extension of filopodia, will be essential for exploiting the therapeutic potential of targeting PECAM-1.