Stanniocalcin, a potential ovarian angiogenesis regulator, does not affect endothelial cell apoptosis.

The ovarian follicle represents an outstanding model for the investigation of the angiogenic process. In fact, follicular development is associated with an extensive neovascularization, and physiological angiogenesis is necessary for folliculogenesis. However, although the major factors triggering the angiogenic events have been thoroughly investigated and are now relatively well defined, information about the molecular events involved in the modulation and/or arrest of neovascularization is still scarce. Therefore, this research focused on the potential involvement of stanniocalcin (STC), a protein whose biological function is still unclear, in the control mechanisms of follicular angiogenesis. We evaluated the effect of 5 and 50 ng/mL STC on the production of the main proangiogenic factor, vascular endothelial growth factor (VEGF), by swine granulosa cells. Moreover, STC's effect on cell viability and the modulation of caspase-3 and -7 activities in swine aortic endothelial cells were also examined. Granulosa cell VEGF production was significantly (P < 0.001) inhibited by STC. Endothelial cell viability was significantly (P < 0.001) increased, whereas caspase activities were reduced (P < 0.01) by STC. These data indicate that STC is not angiosuppressive for endothelial cells, although it could potentially modulate local angiogenesis acting at the granulosa cell level.