Effect of XXXX , @entity1420 and @entity251 on apoptosis- and proliferation-induced MAPK signaling in @entity1 umbilical vein endothelial cells.

@entity1 @entity251 @entity1420 @entity3963 @entity53 @entity4675 @entity1299 @entity204
Sex hormones induce @entity204 or cell proliferation in various cell lines and in primary cultures. However, the signal transduction pathways involved in the regulation of proliferation and apoptosis in endothelial cells have not been fully elucidated. Here, we report that @entity1420 and @entity251 induce apoptosis in HUVECs in a @entity3963 - and @entity4675 -dependent manner, and that @entity53 promotes proliferation via the activation of @entity3963 . We showed that, at physiological doses, @entity1420 and @entity251 promoted @entity3963 , but not @entity4675 , phosphorylation. Hormone inhibitors, on the other hand, prevented @entity3963 phosphorylation. When supraphysiological doses were applied, both @entity3963 and @entity4675 were phosphorylated, causing apoptotic cell @entity204 . The addition of hormone inhibitors at an appropriate concentration did not prevent cell @entity204 or the phosphorylation of @entity3963 and @entity4675 . @entity53 , at physiological doses, promoted an increase in @entity3963 phosphorylation that was blocked by @entity1299 . At physiological and supraphysiological doses, it promoted a proliferative effect. In conclusion, these findings suggest that @entity4675 has an important pro-apoptotic function following @entity1420 and @entity251 treatment in @entity1 endothelial cells, and that @entity3963 has a proliferative effect following @entity53 treatment.
