Fig. 1.

Circulating blood monocytes adhere to activated endothelium at sites of disease or injury. The monocyte becomes polarized and forms a pseudopod in response to a chemical gradient of chemotactic factor production like MCP-1 and follows the increasing concentration of the chemotactic factor into the tissue. PLA₂ translocate to distinct compartments: iPLA₂, PLC, and PLD to the pseudopod at the leading edge and cPLA₂ to the endoplasmic reticulum posterior to the nucleus. LPA is generated by iPLA₂ at the leading edge of the cell where it regulates actin polymerization and protrusion of the pseudopod. LPA also facilitates detection of the MCP-1 gradient since it was shown to regulate not only the speed but also the directionality of monocyte migration. AA is generated by cPLA₂ and regulates the efficiency of monocyte migration through as yet unknown mechanisms. One regulatory role of PLD is its apparent upstream regulation of PA production that serves as a substrate for iPLA₂ generation of LPA. PLC can influence chemotaxis by regulating actin polymerization via the phosphatidyl inositol 3-kinase pathway.