The impact of flutamide on prostaglandin F 2α synthase and prostaglandin F 2α receptor expression, and prostaglandin F 2α concentration in the porcine corpus luteum of pregnancy

Dec 31, 2016Domestic animal endocrinology

Flutamide's effects on prostaglandin production and receptor levels in the pig's pregnancy hormone tissue

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Abstract

Flutamide administration increased progesterone-related factors in the porcine corpus luteum during late pregnancy.

Flutamide upregulated both PGFS mRNA and protein in the corpus luteum on gestational days 90 and 108.
PTGFR mRNA levels increased significantly on gestational day 90, while PTGFR protein levels were higher on both gestational days.
PGFS was localized in the cytoplasm of large luteal cells on gestational day 90, and sparse small luteal cells also exhibited positive staining on day 108.
PTGFR showed membranous localization in large luteal cells across both gestational periods.
Luteal tissue PGF concentration was significantly greater after flutamide treatment on both gestational days compared to control groups.

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Recently, we have indicated that flutamide-induced androgen deficiency diminished progesterone production in the porcine corpus luteum (CL) during late pregnancy and before parturition, as a sign of functional luteolysis. In pigs, the main luteolytic factor is prostaglandin F(PGF), which acts via specific receptors (PTGFRs), and its biosynthesis is catalyzed by prostaglandin Fsynthase (PGFS). The present study investigated the impact of flutamide on luteal PGFS and PTGFR expression, as well as intraluteal PGFcontent during pregnancy in pigs. Flutamide (50 mg/kg BW per day, for 7 d) or corn oil (control groups) were administered subcutaneously into pregnant gilts (n = 3 per group) between 83 and 89 (GD90) or 101-107 (GD108) days of gestation (GD). On GD90 and GD108 ovaries were collected and CLs were obtained. Real-time PCR and Western blot analyses were conducted to quantify PGFS and PTGFR mRNA and protein expression, respectively. In addition, immunohistochemical localization of both proteins was performed and the concentration of PGFwas analyzed by enzyme immunoassay method. Flutamide caused upregulation of PGFS mRNA and protein in GD90F (P = 0.008; P = 0.008, respectively) and GD108F (P = 0.041; P = 0.009, respectively) groups. The level of PTGFR mRNA increased only in the GD90F (P = 0.007) group, whereas PTGFR protein expression was greater in both gestational periods (P = 0.035; P = 0.038, respectively). On GD90 PGFS was immunolocalized in the cytoplasm of large luteal cells only, whereas on GD108, sparse small luteal cells also displayed positive staining. PTGFR showed membranous localization within large luteal cells on both days of pregnancy. In luteal tissue, PGFconcentration was greater after flutamide exposure on both days (P = 0.041; P = 0.038, respectively), when compared with control groups. Overall, the enhanced luteal PGFcontent due to increased PGFS expression after flutamide administration might contribute to premature CL regression. Moreover, higher PTGFR protein levels indicate enhanced sensitivity of luteal cells to PGFunder androgen deficiency. 2α 2α 2α 2α 2α 2α 2α 2α

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The impact of flutamide on prostaglandin F 2α synthase and prostaglandin F 2α receptor expression, and prostaglandin F 2α concentration in the porcine corpus luteum of pregnancy

Abstract

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