The Gαq/11-provoked induction of Akr1c18 in murine luteal cells is mediated by phospholipase C

By measuring the effects of PGF2α on the activation of RhoA (activated by p63RhoGEF) and the effects of activators and inhibitors of RhoA on the PGF2α-induced expression of luteal Akr1c18, we determined that RhoA is neither activated by PGF2α or involved in the PGF2α-induced expression of luteal Akr1c18. The potential involvement of PKCζ was ruled out by the inability of a mutant of a constitutively active Gαq that prevents PKCζ binding to block the increased expression of Akr1c18. Furthermore, PGF2α does not increase the phosphorylation of ERK-5, the only known downstream target of PKCζ. On the other hand, three different mutants of a constitutively active Gαq that prevent phospholipase C activation blocked the induction of luteal Akr1c18. We conclude that the induction of luteal Akr1c18 by Gαq/11 is mediated by the activation of phospholipase C.