Prostaglandin E-2-9-ketoreductase in ovarian tissues

Watson, John; Shepherd, Thomas; Dodson, Kay S.

doi:10.1530/jrf.0.0570489

Cited by 51 publications

(13 citation statements)

References 24 publications

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“…These results may suggest a lack of P4 effect on prostaglandin secretion, in disagreement with what has been shown in bovine CL cells and tissue (Skarzynski and Okuda 1999). Another explanation might be the modulation of PG-converting enzymes activity (Watson et al 1979, Beaver and Murdoch 1992, Asselin and Fortier 2000, Madore et al 2003, the mechanism by which P4 could switch, in the equine CL, from production of luteotrophic PGE2 to luteolytic PGF2α, or vice versa. However, further studies are needed to clarify this hypothesis.…”

Section: Physiological Mechanisms Of Regulation Of CL Formationcontrasting

confidence: 68%

Some aspects of regulation of luteal function and luteolysis in equine corpora lutea

Ferreira‐Dias¹,

Skarzynski²

2008

PHK

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SummaryLike in other mammalian species, in the mare, in every ovarian cycle, a complex process of luteinization leads to corpus luteum (CL) formation. The CL produces progesterone (P4), a required hormone for establishment and maintenance of early pregnancy. Luteal angiogenesis in the mare, necessary for the CL formation, is followed by vascular regression during tissue involution, coordinated with the development and regression of non-vascular tissue (steroidogenic cells included). These processes might be regulated by several factors, still not completely understood. This work reviews some of our studies on this field in the mare. In the equine CL, tumour necrosis factor (TNFα) and nitric oxide (NO) may stimulate the production of angiogenic factor(s) and prostaglandin (PG) E2, necessary for vascular and non-vascular development during the early luteal phase. Increased microvascularization is accompanied by the synthesis of P4, rise in P4 receptor number and an increase in the number of large luteal cells. This suggests the importance of large luteal cells in the auto/paracrine regulation of P4 synthesis in the equine CL. However, when angiogenesis is complete, long term exposure to progestagens appears to inhibit the proliferative/angiogenic activity. PGF2α may also induce luteal (including vascular) regression of the equine CL. Moreover, NO and P4 dependent process of inhibition of angiogenic factor(s) production might be preparing the CL for functional and structural regression. Oppositely to the early luteal phase, during late luteal phase NO and cytokines may induce several processes leading to the regression of equine CL. Besides, caspase-3, the effector enzyme of apoptosis, might also play an important role during luteal tissue involution. Nevertheless, further studies are needed to elucidate the mechanisms and the relationship between the dichotomy of loss of function and/or luteal involution in the mare.

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Section: Physiological Mechanisms Of Regulation Of CL Formationcontrasting

confidence: 68%

Some aspects of regulation of luteal function and luteolysis in equine corpora lutea

Ferreira‐Dias¹,

Skarzynski²

2008

PHK

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“…We were also unable to find evidence for the existence of a 9-keto-reductase enzyme converting PGE 2 to PGF 2rf in either the endometrium or myometrium, although such enzymes have been described in the human ovary (27), human placenta (28), rat heart, brain, and kidney (29), and monkey and pigeon tissues (25). All of these studies were carried out with a more purified enzyme preparation (the 100,000 X g supernatant), and it is possible that any 9-keto-reductase activity is masked in whole tissue homogenates.…”

Section: Discussionmentioning

confidence: 82%

Metabolism of Prostaglandins by the Nonpregnant Human Uterus*

Abel

Kelly

1983

The Journal of Clinical Endocrinology & Metabolism

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We investigated the ability of the nonpregnant human uterus to metabolize prostaglandins E2 and F2 alpha (PGE2 and PGF2 alpha) using radiolabeled substrates together with gas chromatography-mass spectrometry for the measurement of specific metabolites. Both the 15-hydroxyprostaglandin dehydrogenase and the delta 13-reductase enzymes are present in endometrium and myometrium. As shown for other tissues, the dehydrogenase is NAD+ dependent, while the delta 13-reductase requires NADPH as cofactor. PGE2 was the preferred substrate in both tissues; however, the metabolizing capacity of follicular phase myometrium was comparable with that of midluteal phase endometrium. The Km values of the dehydrogenase for PGE2 and PGF2 alpha were similar in both endometrium (1.89 X 10(-6) and 18.52 X 10(-6) mol/liter, respectively) and myometrium (2.76 X 10(-6) and 11.64 X 10(-6) mol/liter, respectively), suggesting that the same enzyme is present in both tissues although the regulation of this enzyme may differ in endometrium and myometrium.

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“…influence ovarian PG concentrations (Watson, Shepherd & Dodson, 1979). The relative contribution of this interconversion in controlling PGE-2 production by the rat ovary has also been investigated.…”

mentioning

confidence: 99%

Studies on ovarian prostaglandin production in relation to ovulation in the rat

Brown¹,

Poyser²

1984

Reproduction

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Prostaglandin (PG) and thromboxane (TX) synthesizing capacities of the rat ovary were measured at 4-h intervals during the 4-day oestrous cycle of the rat. Production of PGE-2, PGF-2 alpha, 6-oxo-PGF-1 alpha and TXB-2 increased 5-fold, 1.6-fold, 1.7-fold and 1.7-fold, respectively, between 18:00 h on the day of pro-oestrus and 02:00 h at oestrus. This preferential stimulation of ovarian PGE-2 production, after the ovulatory surge of LH before ovulation, provides further evidence for the involvement of ovarian PGE-2 in ovulation in the rat. These increases in ovarian PG production were not due to differences in arachidonic acid availability, PG metabolism, or the interconversion of PGE-2 and PGF-2 alpha. In addition, the greater stimulation of PGE-2 synthesis was not due to an increase in PGH-2 to PGE-2 synthetase activity. It is concluded that the ovulatory LH surge late in the afternoon of pro-oestrus in the rat causes an increase in ovarian cyclo-oxygenase (PGH-2 synthetase) activity with the majority of the PGH-2 synthesized being directed into the PGE-2-forming pathway.

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Prostaglandin E-2-9-ketoreductase in ovarian tissues

Abstract: Summary. The existence of the enzyme prostaglandin E-2-9-ketoreductase which can convert prostaglandin E-2 to prostaglandin F-2\g=a\was

Cited by 51 publications

References 24 publications

Some aspects of regulation of luteal function and luteolysis in equine corpora lutea

Some aspects of regulation of luteal function and luteolysis in equine corpora lutea

Metabolism of Prostaglandins by the Nonpregnant Human Uterus*

Studies on ovarian prostaglandin production in relation to ovulation in the rat

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