H-2g induces HMVEC chemotaxis through JAK2 and PI3K pathways but not through Src and MAPK. (A) H-2g induced a dose-dependent increase in HMVEC chemotaxis compared with negative control PBS. (B) For inhibition studies, HMVECs were pretreated with the chemical inhibitors (50 μM AG490, 20 μM LY294002, 20 μM PD98059, or 20 μM PP2) for 2 hours at 37°C and then assayed in 48-well chemotaxis chambers in response to 100 nM of H-2g. H-2g induced HMVEC chemotaxis through the JAK2 and PI3K pathways. (C) HMVECs were transfected with JAK2, Src, PI3K, and Erk1/2 sense (▪) or antisense (□) ODNs. The data confirmed that JAK2 and PI3K are involved in H-2g–induced HMVEC chemotaxis, but Src and MAPK are not. Results are expressed as the number of cells migrating through the membrane per well plus or minus the standard error of the mean (SEM) from 6 independent experiments. ^*Represents a significant difference (^*P < .05) between the respective groups.