Abstract
The aim of this study was to investigate about endothelial cell injury caused by hypoxia or hypoxia/reoxygenation and the effect of PGE1 on the injury using human umbilical vein endothelial cells (HUVEC) .Under hypoxia, HUVEC shrank and peeled from dish, accompanied with reduced thymidine uptake, induced DNA fragmentation, and increased caspase-3 activity. On the other hand, under reoxygenation after hypoxia, HUVEC restarted proliferation as a result of decreasing caspase-3 activity in a time dependent manner.When PGE1 was added prior to hypoxia, the number of living cells got fewer and caspase-3 activity was potentiated without changing of cAMP levels. In contrast, the addition of PGE1 just before reoxygenation, increased the number of living cells and decreased caspase-3 activity with increasing cAMP levels. Under neither hypoxia nor reoxygenation, the gene expression of any prostaglandin EP receptors was not observed. In conclusion, PGE1 showed opposite effects to be pro-apoptotic under hypoxia, and to be anti-apoptotic under reoxygenation, not through EP receptors.
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