Rat corneal endothelial cell migration during wound repair on the basement membrane depends more on the PI-3K pathway than the cdc-42 pathway or actin stress fibers.

摘要: Following a central transcorneal circular freeze injury, organ-cultured rat corneal endothelial cells surrounding the wound reorganize peripheral actin bands into stress fibers and migrate individually wound. To ascertain significance of this rearrangement relative to morphological changes accompanying migration repair, some tissues were incubated overnight in 4 μM TRITC-conjugated phalloidin stabilize prevent its reorganization. After injury endothelium histologically observed at 24 h post-wounding demonstrated that despite lack organization, responding appeared morphologically similar their control counterparts. Tissues cultivated presence either cytochalasin B (CB), soybean agglutinin (SBA), or fluorouracil (FU) also exhibited cytoskeletal disruption. Under these conditions, continued absence detectable fibers. For SBA-, CB-, FU-treated tissues, repair did not significantly differ from preparations although showed slower repair. Electron micrographs confirmed an migrating treated with any agents. ML 141 EY294002 inhibit cdc-42 PI-3K pathways, respectively. While cell movement still occurred 141, was greatly restricted EY294002. These results indicate situ does require reorganization fibers, but functioning pathway is indispensable for along basement membrane during