A clinically relevant mouse model of human multiple myeloma ?

pletely inhibit EVT migration, plateletderived soluble factors other than chemokines most likely also play a role in EVT migration. Though other studies have suggested that a lipid mediator, sphingosine-1-phosphate (S1P), is released from platelets,4 Sato and colleagues found that lipid removal from platelet-CM by charcoal stripping did not affect migration. However, heat inactivation of peptides halted migratory activity, indicating that protein factors, such as chemokines, are the premier factors in promotion of EVT migration. These findings suggest that platelet activation and release of chemoattractants, triggered by contact with the ECM of invading EVTs, set off a positive feedback loop that promotes further EVT infiltration to maternal spiral arteries. Abundant expression on trophoblasts of thrombomodulin and tissueand urokinase-type tissue plasminogen activators may ensure that abnormal coagulation does not occur during this process. Greater understanding of the reciprocal regulation between platelets and EVTs may help develop more targeted therapies for preeclampsia, pregnancy loss, and fetal growth retardation. ■