11-deoxy prostaglandin F(2α), a thromboxane A2 receptor agonist, partially alleviates embryo crowding in Lpar3((-/-)) females

Abstract

Objective: To determine cyclooxygenase-derived prostanoid signaling in alleviating embryo crowding in the Lpar3((-/-)) females.

Design: Experimental mouse model.

Setting: Research laboratories.

Animal(s): Wild-type, Lpar3((+/-)), and Lpar3((-/-)) mice.

Intervention(s): Intraperitoneal (IP) administration of prostaglandin E(2) (PGE(2)), cPGI (a stable analogue of PGI(2)), and 11-deoxy prostaglandin F(2α) (11-deoxy PGF(2α), a thromboxane A(2) receptor agonist) to preimplantation gestation day 3.5 Lpar3((-/-)) females.

Main outcome measure(s): Implantation sites were detected by blue dye reaction and embryo spacing was determined by the distribution of the implantation sites along the uterine horns on gestation day 4.5; pregnancy outcome was measured by litter size at birth.

Result(s): Administration of PGE(2) + cPGI on gestation day 3.5 Lpar3((-/-)) females restored on-time implantation but did not affect embryo spacing or the number of implantation sites detected on gestation day 4.5; PGE(2) + cPGI treatment increased litter size at birth. Administration of PGE(2) + cPGI + 11-deoxy PGF(2α) on gestation day 3.5 Lpar3((-/-)) females rescued on-time implantation, partially dispersed the clustered implantation sites normally observed in the Lpar3((-/-)) females, increased the number of implantation sites detected on gestation day 4.5, and increased litter size at birth.

Conclusion(s): The thromboxane A(2) receptor agonist 11-deoxy PGF(2α) can partially alleviate embryo crowding in the Lpar3((-/-)) females and embryo crowding likely contributes to reduced litter size in the Lpar3((-/-)) females.