Stimulation of XXXX formation mediated through the prostaglandin EP2 receptor in @entity35 luteal endothelial cells.

@entity4665 @entity18518 @entity2508 @entity43507 @entity1421 @entity5274 @entity1919 @entity35 @entity9501 @entity6667
To explore the role of @entity1421 ( @entity1421 ) in angiogenesis in the developing corpus luteum, luteal microvascular endothelial-like cells (luteal ECs) were prepared from highly luteinizing ovaries of @entity35 using the percoll density gradient method. The cells abundantly expressed the mRNAs of the endothelial markers @entity18518 ( @entity18518 ) and responded to the @entity6667 ( @entity6667 ) to form in vitro @entity5274 structures on Matrigel. Cyclooxygenase (COX) inhibitors significantly suppressed @entity5274 formation in luteal ECs, whereas @entity1421 counteracted the COX inhibitor-induced blockage. @entity1421 -induced @entity5274 formation was blocked by a @entity1919 -dependent protein kinase A (PKA) inhibitor, @entity9501 . The antagonist against the PGE receptor type 2 (EP2 receptor), @entity43507 , completely inhibited @entity1421 -induced @entity5274 formation and partly suppressed the @entity6667 -induced @entity5274 formation but did not attenuate @entity1421 -induced phosphorylation of both AKT kinase and @entity2508 . @entity6667 significantly enhanced the expression of @entity4665 mRNAs detected by real-time RT-PCR and @entity1421 secretion into the media measured by ELISA in luteal ECs. In turn, @entity1421 stimulated @entity6667 expression. In vitro co-culture of luteal ECs with steroidogenic luteal cells (SLCs) promoted @entity5274 formation. Pre-treatment of SLCs with @entity6667 further enhanced @entity5274 formation of ECs, and this effect was blocked by the @entity4665 inhibitor. This stimulatory effect was inhibited by treatment with @entity43507 . These data indicate that @entity1421 exerts a direct stimulatory effect on @entity5274 formation mainly via the EP2 receptor/PKA signaling in luteal ECs. Our results suggest the possibility that the endogenous @entity1421 that is produced from luteinizing follicular cells as well as ECs may stimulate luteal angiogenesis.
