Biosynthesis and catabolism of prostaglandin F2(alpha) (PGF2α) are controlled by progesterone in the rat uterus during pregnancy

Farina, Mariana; Ribeiro, Maria L.C.; Weissmann, Carina; Estévez, Alejandra; Billi, Silvia; Vercelli, Claudia Alejandra; Franchi, A.M.

doi:10.1016/j.jsbmb.2004.05.001

Cited by 29 publications

(33 citation statements)

References 24 publications

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“…As we have mentioned before, in the rat, P maintains uterine quiescence during gestation and decreases at term, allowing for the increase in the synthesis of PGs involved in the onset of labor (15). The pattern of EGF in the AF showed an inverse correlation when compared with P. Thus, our results suggest that endogenous EGF could be responsible for a mechanism that maintains the function of the CL.…”

Section: Discussionsupporting

confidence: 75%

“…Because PGF 2␣ decreased and P increased after EGF treatment, we assessed whether any effect occurred with regard to CL morphology. Eight hours after EGF administration, the CL seemed to be reluteinized; their appearance was similar to that of CL obtained from control rats on d13 of pregnancy when P was maximum (15).…”

Section: Discussionsupporting

confidence: 70%

“…5A). This image corresponded to cytoplasms with a high concentration of lipid droplets, suggesting very active P synthesis (15). Their nuclei were eccentric and basophilic.…”

Section: Resultsmentioning

confidence: 89%

“…4). Control rats on d13 of pregnancy were included because we observed the highest P level at this time during gestation (15). Ovaries from control rats on d13 of pregnancy presented big CL, follicles in different developmental stages, and typical blood vessels (Fig.…”

Section: Resultsmentioning

confidence: 97%

“…At term, CL regression, known as luteolysis, is followed by a decrease in serum P resulting in parturition (14). Near term, cyclooxygenase I (COX-I) expression is augmented in the rat uterus (15). It is thought that luteolysis is caused by this early increase in COX-I followed by an increase in prostaglandin F 2␣ (PGF 2␣ ) secretion (16).…”

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confidence: 99%

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Epidermal growth factor prevents prepartum luteolysis in the rat

Ribeiro¹,

Aisemberg²,

Billi³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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We have previously reported that intrauterine (i͞u) administration of epidermal growth factor (EGF 500 ng) on day (d) 21 of pregnancy delayed 19.0 ؎ 0.6 h the onset of labor. Progesterone (P) is secreted by ovarian corpora lutea (CL) throughout gestation in the rat. Prepartum CL regression due to increased uterine cyclooxygenase I and prostaglandin F 2␣ results in P withdrawal followed by labor. The aims of the present work were (i) to study whether EGF delayed-onset of labor was mediated by a mechanism that prevented CL regression; (ii) to determine amniotic fluid (AF) EGF in pregnant rats. Rats on d21 of pregnancy received i͞u EGF (500 ng) and were killed 0, 4, 8, 12, 24, and 48 h later. Control AF from rats on d13 and 18 -22 of pregnancy was obtained. EGF decreased uterine prostaglandin F 2␣ synthesis 8 h after treatment. Twelve hours after EGF injection, P reached its highest serum level and uterine cyclooxygenase I expression was undetectable. CL from rats killed 8 and 12 h after EGF were similar to those from rats on d13 of pregnancy, when serum P is maximum. EGF in AF increased throughout gestation, reached a maximum on d21, and decreased before the onset of labor. We suggest that the effect of EGF on the onset of labor was mediated by an early effect on the uterus that prevented prepartum CL regression.

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Section: Discussionsupporting

confidence: 75%

Section: Discussionsupporting

confidence: 70%

“…5A). This image corresponded to cytoplasms with a high concentration of lipid droplets, suggesting very active P synthesis (15). Their nuclei were eccentric and basophilic.…”

Section: Resultsmentioning

confidence: 89%

Section: Resultsmentioning

confidence: 97%

mentioning

confidence: 99%

See 3 more Smart Citations

Epidermal growth factor prevents prepartum luteolysis in the rat

Ribeiro¹,

Aisemberg²,

Billi³

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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Role of intraluteal and intrauterine prostaglandin signaling in LH‐induced luteolysis in pregnant rats

Vashistha

Khan

2023

Molecular Reproduction Devel

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Luteal dysfunctions lead to fertility disorders and pregnancy complications. Normal luteal function is regulated by many factors, including luteinizing hormone (LH). The luteotropic roles of LH have been widely investigated but its role in the process of luteolysis has received little attention. LH has been shown to have luteolytic effects during pregnancy in rats and the role of intraluteal prostaglandins (PGs) in LH‐mediated luteolysis has been demonstrated by others. However, the status of PG signaling in the uterus during LH‐mediated luteolysis remains unexplored. In this study, we utilized the repeated LH administration (4×LH) model for luteolysis induction. We have examined the effect of LH‐mediated luteolysis on the expression of genes involved in luteal/uterine PG synthesis, luteal PGF2α signaling, and uterine activation during different stages (mid and late) of pregnancy. Further, we analyzed the effect of overall PG synthesis machinery blockage on LH‐mediated luteolysis during late pregnancy. Unlike the midstage of pregnancy, the expression of genes involved in PG synthesis, PGF2α signaling, and uterine activation in late‐stage pregnant rats' luteal and uterine tissue increase 4×LH. Since the cAMP/PKA pathway mediates LH‐mediated luteolysis, we analyzed the effect of inhibition of endogenous PG synthesis on the cAMP/PKA/CREB pathway, followed by the analysis of the expression of markers of luteolysis. Inhibition of endogenous PG synthesis did not affect the cAMP/PKA/CREB pathway. However, in the absence of endogenous PGs, luteolysis could not be activated to the full extent. Our results suggest that endogenous PGs may contribute to LH‐mediated luteolysis, but this dependency on endogenous PGs is pregnancy‐stage dependent. These findings advance our understanding of the molecular pathways that regulate luteolysis.

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Two-step inhibitory effect of kanzo on oxytocin-induced and prostaglandin F2α-induced uterine myometrial contractions

et al. 2014

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We previously reported that shakuyaku-kanzo-to, a kampo medicine consisting of shakuyaku and kanzo, has an inhibitory effect on myometrial contractions in pregnant women. In this study, we evaluated the effects of kanzo, glycyrrhizin (a major component of kanzo), glycyrrhetinic acid (GA; a major metabolite of glycyrrhizin), shakuyaku, and paeoniflorin (a major component of shakuyaku) on agonist-induced contractions of the uterus of pregnant humans and rats. We prepared myometrial strips from the uterus of pregnant humans and rats and induced contractions with oxytocin (50 μU/mL) or prostaglandin F2α (PGF2α) (10(-7) or 10(-6) M). Kanzo (250 μg/mL) and GA (5 × 10(-6) M) inhibited the oxytocin-induced and PGF2α-induced contractions in pregnant human and rat myometrium, but shakuyaku (250 μg/mL), paeoniflorin (10(-5) M), and glycyrrhizin (10(-5) M) did not inhibit contractions in either. Interestingly, kanzo and GA showed an inhibitory effect after temporarily enhancing the PGF2α-induced contractions in the rat myometrium, but not in the human myometrium. These results suggest that kanzo has at least a two-step inhibitory effect on the myometrial contractions that originate from the kanzo itself and a metabolite of glycyrrhizin in kanzo. Furthermore, kanzo was found to be safe for inhibiting PGF2α-induced contractions in humans because it did not temporarily enhance PGF2α-induced contractions.

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Biosynthesis and catabolism of prostaglandin F2(alpha) (PGF2α) are controlled by progesterone in the rat uterus during pregnancy

Cited by 29 publications

References 24 publications

Epidermal growth factor prevents prepartum luteolysis in the rat

Epidermal growth factor prevents prepartum luteolysis in the rat

Role of intraluteal and intrauterine prostaglandin signaling in LH‐induced luteolysis in pregnant rats

Two-step inhibitory effect of kanzo on oxytocin-induced and prostaglandin F2α-induced uterine myometrial contractions

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