Endothelial migration is one of the major events of pathological neovascula
rization. We compared the characteristics of Ca2+ mobilization in nonconflu
ent, confluent, and migrating endothelial cells. Migration of endothelial c
ells was induced by wounding the confluent cell monolayer. The basal intrac
ellular Ca2+ concentration was lower in migrating cells and higher in confl
uent cells than in nonconfluent cells. Thapsigargin (TG)-induced Ca2+ leak
and TG-evoked Ca2+ entry were accelerated in migrating cells, whereas the l
atter was suppressed in confluent cells. The ATP-induced Ca2+ transient was
also much larger in migrating cells than in confluent cells. These alterat
ions were also observed in a cell as an intracellular polarization, i.e., t
he leading edge showed an acceleration of TG-evoked Ca2+ entry and an augme
ntation of the ATP-induced Ca2+ transient. Endothelial migration was signif
icantly suppressed by TG or cyclopiazonic acid. These observations suggest
that the alterations of Ca2+ store site-related Ca2+ mobilizations, i.e., C
a2+ sequestration, release, and TG-evoked Ca2+ entry, may be involved in th
e cellular mechanisms of endothelial migration.