Journal article
Activation of Gq/11 in the mouse corpus luteum is required for parturition
Molecular endocrinology (Baltimore, Md.), Vol.29(2), pp.238-246
02/2015
DOI: 10.1210/me.2014-1324
PMCID: PMC4318882
PMID: 25495873
Abstract
Mice with a deletion of Gα(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 Gα(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)α, because this hormone is known to activate phospholipase C (a prominent Gα(q/11) effector) in luteal cells and because the action of PGF2α on luteal cells is the first step in the murine parturition pathway. Our data show that the conditional deletion of Gα(q/11) from granulosa cells prevents the ability of PGF2α to induce Akr1c18 in luteal cells. Akr1c18 codes for 20α-hydroxysteroid dehydrogenase, an enzyme that inactivates progesterone. The PGF2α-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 Gαq/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 Gα(q/11) from granulosa cells.
Details
- Title: Subtitle
- Activation of Gq/11 in the mouse corpus luteum is required for parturition
- Creators
- Rachel Mejia - University of Iowa, Carver College of MedicineCourtney WaiteMario Ascoli - University of Iowa, Carver College of Medicine
- Resource Type
- Journal article
- Publication Details
- Molecular endocrinology (Baltimore, Md.), Vol.29(2), pp.238-246
- DOI
- 10.1210/me.2014-1324
- PMID
- 25495873
- PMCID
- PMC4318882
- NLM abbreviation
- Mol Endocrinol
- ISSN
- 0888-8809
- eISSN
- 1944-9917
- Publisher
- United States
- Grant note
- K12 HD063117 / NICHD NIH HHS
- Language
- English
- Date published
- 02/2015
- Academic Unit
- Obstetrics and Gynecology; Neuroscience and Pharmacology
- Record Identifier
- 9983930397702771
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