Prostaglandin F-2  receptors in corpora lutea of pregnant rats and relationship with induction of 20 -hydroxysteroid dehydrogenase

Bussmann, Leonardo E.

doi:10.1530/jrf.0.0850331

Cited by 19 publications

(13 citation statements)

References 23 publications

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“…Indeed, inhibition of steroidogenesis does not initiate luteal regression or augment PRL-induced luteal regression in the hypophysectomized rat [58]. Similar to the current study, inhibition of FP receptor mRNA by PGF has been reported in sheep, cow, and human cells [59][60][61][62][63], and PGF binding to rat luteal cells is reduced following PGF treatment [64]. In contrast, Olofsson and colleagues [65] report that PGF increases FP receptor mRNA concentrations in rats.…”

Section: Discussionsupporting

confidence: 81%

Actions of Prostaglandin F2α and Prolactin on Intercellular Adhesion Molecule-1 Expression and Monocyte/Macrophage Accumulation in the Rat Corpus Luteum1

Olson

Anderson

Wiltbank

et al. 2001

Biology of Reproduction

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Expression of intercellular adhesion molecule-1 (ICAM-1) and the accumulation of monocytes/macrophages are inflammatory events that occur during PRL (PRL)-induced regression of the rat corpus luteum. Here we have compared the ability of prostaglandin F2alpha (PGF) and PRL to induce, in rat corpora lutea, inflammatory events thought to perpetuate luteal regression. Immature rats were ovulated with eCG-hCG and then hypophysectomized (Day 0), which resulted in a single cohort of persistent, functional corpora lutea. On Days 9-11, the rats received twice daily injections of saline, PGF (Lutalyse, 250 microg/injection), or PRL (312 microg/injection) to induce luteal regression. Surprisingly, luteal weight and plasma progestin concentrations (progesterone and 20alpha-dihydroprogesterone) did not differ between PGF-treated rats and controls; whereas both luteal weight and plasma progestins declined significantly in PRL-treated rats. Furthermore, corpora lutea of PGF-treated rats and controls contained relatively minimal ICAM-1 staining and few monocytes/macrophages. In contrast, but as expected, corpora lutea of PRL-treated rats stained intensely for ICAM-1 and contained numerous monocytes/macrophages. In an additional experiment, there was no indication that luteal prostaglandin F2alpha receptor mRNA diminished as a result of hypophysectomy. These findings suggest that prolactin, not PGF, induces the inflammatory events that accompany regression of the rat corpus luteum.

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Section: Discussionsupporting

confidence: 81%

Actions of Prostaglandin F2α and Prolactin on Intercellular Adhesion Molecule-1 Expression and Monocyte/Macrophage Accumulation in the Rat Corpus Luteum1

Olson

Anderson

Wiltbank

et al. 2001

Biology of Reproduction

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“…Another factor to be considered is a change in the sensitivity of the CL to PGF 2 with advancing gestation (Vermouth & Deis 1975, Khan et al 1979, Lahav et al 1988. Recent reports indicate that the number of PGF 2 binding sites increased with the age of the CL (Bussmann 1989, Orlicky et al 1992.…”

Section: Discussionmentioning

confidence: 99%

“…Administration of PGF 2 induces abortion (Deis 1971), and induction of 20 -hydroxysteroid dehydrogenase (20 -HSD) activity (Pharriss & Wyngarden 1969, Strauss & Stambaugh 1974, Lamprecht et al 1975, Bussmann & Deis 1979, an enzyme that converts P 4 into a derivative devoid of progestational activity and considered a marker of luteolysis (Wiest 1968. The role of PGF 2 as an inducer of the physiological luteolysis in the rat is corroborated by the demonstration of specific receptors for PGF 2 on luteal membranes (Wright et al 1979, Bussmann 1989). Locally synthesised PGs have an important role in CL regression as indicated by an increase in the content of PGF 2 in the CL during spontaneous luteolysis (Olofsson & Selstam 1988).…”

Section: Introductionmentioning

confidence: 96%

“…P 4 alters the synthesis of luteal PGs (Pate 1988), which may be modulators of luteal steroidogenesis (Olofsson & Leung 1994). On the other hand, in luteolysis preceding normal parturition , Lacy et al 1976, or induced by PGF 2 (Bussmann 1989) or LH (Stocco & Deis 1996), the decrease in P 4 content in luteal cells precedes the increase in 20 -HSD activity.…”

Section: Introductionmentioning

confidence: 99%

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Participation of intraluteal progesterone and prostaglandin F2 alpha in LH-induced luteolysis in pregnant rat

Stocco

Deis

1998

Journal of Endocrinology

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We examined the participation of the intraluteal levels of progesterone (P 4 ) and prostaglandin F 2 (PGF 2 ) in the induction of luteolysis by LH and its relationship with the induction of the 20 -hydroxysteroid dehydrogenase activity (20 -HSD). Subcutaneous administration of four doses of 10 µg ovine LH (oLH) at 0800, 0900, 1000 and 1100 h on day 19 of pregnancy induced a decrease in the activity of the enzyme 3 -HSD 24 and 48 h after treatment and an increase in luteal 20 -HSD activity 48 h after oLH treatment when compared with control rats. Intraluteal and serum P 4 levels were lower than control values 24 and 48 h after oLH treatment, with a significant increase in luteal PGF 2 content and a decrease in corpus luteum (CL) weight 48 h after oLH treatment. Intrabursal ovarian (IB) treatment with an inhibitor of PG's biosynthesis (diclofenac) (70 µg/ovary) or P 4 (3 µg/ovary) on day 20 of pregnancy, prevented the increase in 20 -HSD activity observed 48 h after oLH treatment, without any effect on 3 -HSD activity. The IB administration of P 4 prevented the increase in intraluteal PGF 2 content induced by oLH treatment and the increases in 20 -HSD activity and intraluteal PGF 2 content observed in control animals on day 21 of pregnancy. The inhibition of PG biosynthesis also prevents the decrease in intraluteal and serum P 4 level induced by oLH. These results provide good evidence of the important participation of intraluteal P 4 and PGF 2 on the oLH-induced luteolysis in pregnant rats. We also found that P 4 produced by the CL is involved, in part, in the regulation of luteal PG synthesis. Thus, the early decline in 3 -HSD activity and the consequent fall in intraluteal P 4 content, may trigger the synthesis of PGs and thereafter the increase in luteal 20 -HSD activity to establish luteolysis.

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“…E2 also modified the expression of anti-apoptotic BCLl-2 and pro-apoptotic BAX (BCL2-associated X protein) genes, which are critical regulators of cell survival and death . During mid-pregnancy in rats, E2 is required for luteal survival, whereas at the end of pregnancy, high serum concentrations are responsible for increased synthesis of prostaglandin F2α and luteal expression of prostaglandin F2α receptors in association with functional regression of the corpora lutea (GIBORI et al, 1984;BUSSMANN, 1989;MCLEAN et al, 1989;. The findings support the premise that this E2 plays important roles in female reproduction.…”

Section: Introductionsupporting

confidence: 64%

O papel do 17β-estradiol no processo luteolítico de cadelas não prenhes

Neto¹,

Pereira²

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O 17β-estradiol (E2) desempenha um papel importante na função reprodutora e na fertilidade feminina, porém, sua ação é estendida para a maioria dos tecidos. Sabendo que o E2 tem funções pleiotrópicas em diferentes tecidos e órgãos, e que pode estar envolvido tanto na proliferação como na morte celular, nossa hipótese é que o E2 seja um dos iniciadores de regressão luteínica em cadelas não prenhes. Para testar nossa hipótese, foram usados corpos lúteos (CL) provenientes de 28 cadelas nos dias 10, 20, 30, 40, 50, 60, 70 The 17β-estradiol (E2) plays an important role in the reproductive function and female fertility, however, its action is extended to most tissues. Knowing that E2 has pleiotropic roles in different organs and tissues, and that might be involved in both cell death and proliferation, our hypothesis is that E2 is one of the triggers of luteal regression in non-pregnant bitches. To

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Prostaglandin F-2 receptors in corpora lutea of pregnant rats and relationship with induction of 20 -hydroxysteroid dehydrogenase

Cited by 19 publications

References 23 publications

Actions of Prostaglandin F2α and Prolactin on Intercellular Adhesion Molecule-1 Expression and Monocyte/Macrophage Accumulation in the Rat Corpus Luteum1

Actions of Prostaglandin F2α and Prolactin on Intercellular Adhesion Molecule-1 Expression and Monocyte/Macrophage Accumulation in the Rat Corpus Luteum1

Participation of intraluteal progesterone and prostaglandin F2 alpha in LH-induced luteolysis in pregnant rat

O papel do 17β-estradiol no processo luteolítico de cadelas não prenhes

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