| First Author | Mejia R | Year | 2015 |
| Journal | Mol Endocrinol | Volume | 29 |
| Issue | 2 | Pages | 238-46 |
| PubMed ID | 25495873 | Mgi Jnum | J:223256 |
| Mgi Id | MGI:5648598 | Doi | 10.1210/me.2014-1324 |
| Citation | Mejia R, et al. (2015) Activation of Gq/11 in the mouse corpus luteum is required for parturition. Mol Endocrinol 29(2):238-46 |
| abstractText | Mice with a deletion of Galpha(q/11) in granulosa cells were previously shown to be subfertile. They also have a reduced ovulatory response due to a deficiency in the ability of the activated LH receptor to fully induce the granulosa cell progesterone receptor. Because this conditional deletion of Galpha(q/11) will interfere with the actions of any G protein-coupled receptor that activates G(q/11) in granulosa or luteal cells, we sought to determine whether the actions of other hormones that contribute to fertility were also impaired. We focused our attention on prostaglandin F2 (PGF2)alpha, because this hormone is known to activate phospholipase C (a prominent Galpha(q/11) effector) in luteal cells and because the action of PGF2alpha on luteal cells is the first step in the murine parturition pathway. Our data show that the conditional deletion of Galpha(q/11) from granulosa cells prevents the ability of PGF2alpha to induce Akr1c18 in luteal cells. Akr1c18 codes for 20alpha-hydroxysteroid dehydrogenase, an enzyme that inactivates progesterone. The PGF2alpha-mediated induction of this enzyme towards the end of pregnancy increases the inactivation of progesterone and precipitates parturition in mice. Thus, the conditional deletion of Galphaq/11 from granulosa/luteal cells prevents the progesterone withdrawal that occurs at the end of pregnancy and impairs parturition. This novel molecular defect contributes to the subfertile phenotype of the mice with a deletion of Galpha(q/11) from granulosa cells. |
