Progesterone and Estrogen Control of Uterine Prostaglandin Dehydrogenase Activity During Deciduomal Growth

Alam, Nargis A.; Russel, Paul; Tabor, M. Wilson; Moulton, Bruce C.

doi:10.1210/endo-98-4-859

Cited by 43 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The present results may be combined with those reported previously for progesterone effects on PGDH (16,(42)(43)(44)(45), to develop a scheme by which PGDH expression and activity in chorion and placental trophoblasts may reflect a balance between opposing influences of cortisol and progesterone (Fig. 5, A and B).…”

Section: Discussionsupporting

confidence: 73%

Local Modulation by 11 -Hydroxysteroid Dehydrogenase of Glucocorticoid Effects on the Activity of 15-Hydroxyprostaglandin Dehydrogenase in Human Chorion and Placental Trophoblast Cells

Patel¹

1999

Journal of Clinical Endocrinology & Metabolism

View full text Add to dashboard Cite

NAD+-dependent 15-hydroxy-PG dehydrogenase (PGDH) is the major enzyme involved in the initial inactivation of PGs, and its activity is reduced by glucocorticoids, cortisol (F), and dexamethasone (DEX). In turn, glucocorticoid regulation of PGDH activity in placenta and chorion could be regulated indirectly by 11beta-hydroxysteroid dehydrogenase (11beta-HSD) activity. In the placenta, 11beta-HSD2 is the dominant isoform, acting as a dehydrogenase [F to cortisone (E)]; and in chorion, 11beta-HSD1 predominates as a reductase (E to F). The present study was designed to determine whether glucocorticoid regulation of PGDH activity in placenta and chorion could be regulated indirectly by 11beta-HSD activity. We obtained Percoll-purified human placental and chorion trophoblast cells from uncomplicated term pregnancies, cultured them for 72 h, then treated the cells with cortisol (100 nmol/L), cortisone (1 micromol/L), or DEX (100 nmol/L), in the presence or absence of carbenoxolone (CBX, 800 nmol/L), an 11beta-HSD inhibitor, for 24 h. Activity of PGDH was assessed by incubation (4 h) with PGF2alpha (282 nmol/L) and measurement of conversion to 13,14-dihydro-15-keto PGF2alpha. CBX alone had no effect on PGDH activity in either placenta or chorion trophoblast cells. In chorion, E significantly inhibited PGDH activity, and this effect was reversed by addition of CBX. F and DEX significantly inhibited PGDH, and this effect was unaltered by coadministration of CBX. In contrast, in placenta, there was no effect of E, or of E with CBX, on PGDH activity. However, F and DEX inhibited PGDH, and the effect of F (but not DEX) was greater in the presence of CBX. In conclusion, we suggest that effects of E and F on PGDH are modified by the tissue-specific expression of 11beta-HSD isoforms.

show abstract

Section: Discussionsupporting

confidence: 73%

Local Modulation by 11 -Hydroxysteroid Dehydrogenase of Glucocorticoid Effects on the Activity of 15-Hydroxyprostaglandin Dehydrogenase in Human Chorion and Placental Trophoblast Cells

Patel¹

1999

Journal of Clinical Endocrinology & Metabolism

View full text Add to dashboard Cite

show abstract

“…In our results, the white matter properties of the cingulum bundle during the periovulatory phase were significantly correlated with the intensity of menstrual pain as rated by patients during the subsequent menstrual period. As we know, one of the main factors responsible for the pathogenesis of PD is the overproduction of uterine PGs [Dawood, ] which are controlled by both estrogen and progesterone [Alam et al, ; Castracane and Jordan, ]. Animal studies demonstrated that estrogen and progesterone could stimulate neurite outgrowth, synapse number, dendritic branching and myelination [Cooke and Woolley, ; Sá et al, ], forming the basis of white matter connectivity in the central nervous system [Peper et al, ].…”

Section: Discussionmentioning

confidence: 99%

Altered white matter microarchitecture in the cingulum bundle in women with primary dysmenorrhea: A tract-based analysis study

Liu

et al. 2017

Hum. Brain Mapp.

View full text Add to dashboard Cite

Primary dysmenorrhea (PD), as characterized by painful menstrual cramps without organic causes, is associated with central sensitization and brain function changes. Previous studies showed the integrated role of the default mode network (DMN) in the pain connectome and its key contribution on how an individual perceives and copes with pain disorders. Here, we aimed to investigate whether the cingulum bundle connecting hub regions of the DMN was disrupted in young women with PD. Diffusion tensor imaging was obtained in 41 PD patients and 41 matched healthy controls (HC) during their periovulatory phase. The production of prostaglandins (PGs) was obtained in PD patients during their pain-free and pain phases. As compared with HC, PD patients had similar scores of pain intensity, anxiety, and depression in their pain-free phase. However, altered white matter properties mainly located in the posterior section of the cingulum bundle were observed in PD. Besides PGs being related to menstrual pain, a close relationship was found between the white matter properties of the cingulum bundle during the pain-free phase and the severity of the menstrual pain in PD patients. Our study suggested that PD had trait changes of white matter integrities in the cingulum bundle that persisted beyond the time of menstruation. We inferred that altered anatomical connections may lead to less-flexible communication within the DMN, and/or between the DMN and other pain-related brain networks, which may result in the central susceptibility to develop chronic pain conditions in PD's later life. Hum Brain Mapp 38:4430-4443, 2017. © 2017 Wiley Periodicals, Inc.

show abstract

“…PGDH is high in secretory phase endometrium and probably never falls in a pregnant cycle and is certainly high in early pregnancy decidua (Keirse and Turnbull, 1975;Keirse, 1985). PGDH may be under progesterone control (Casey et al, 1980;Alam et al, 1975;Falkay and Sas, 1987;Bedwani and Marley, 1975) and it is not surprising that RU486 reduces the activity of this enzyme, which has a short half-life (Xun et al, 1991), and thus is well placed as a key controller of prostaglandin concentration. The result of a decrease in PGDH activity would be both an increase in sensitivity to exogenous prostaglandin (Swahn and Bygdeman, 1988), because of reduced catabolism, and an increased effectiveness of prostaglandin produced within the amnion or decidua (Mitchell et al, 1978).…”

Section: Discussionmentioning

confidence: 99%

The effects of mifepristone (RU486) on prostaglandin dehydrogenase in decidual and chorionic tissue in early pregnancy

Cheng¹,

Kelly²,

Thong

et al. 1993

Human Reproduction

View full text Add to dashboard Cite

Prostaglandin dehydrogenase is the main inactivating enzyme for prostaglandins and therefore controls local levels of prostaglandins. Since there is some evidence that the expression of this enzyme is under progesterone control it is reasonable that one of the effects of antiprogestin is to reduce the concentration of this enzyme and thus increase the effective concentration of prostaglandin within tissue. We have investigated the amount of enzyme activity within decidua and chorionic villi from women receiving the antigestagen mifepristone (RU486) 12, 24 and 36 h prior to surgical abortion, and examined the effect on tissue concentrations of prostaglandin dehydrogenase. Women receiving mifepristone in all groups had a significant reduction in concentration of prostaglandin dehydrogenase enzyme in decidual tissue. There was also a marked reduction in prostaglandin dehydrogenase in decidual cells following RU486, as demonstrated by immunochemical methods. At this stage of pregnancy, prostaglandin dehydrogenase was present in abundance in cytotrophoblast cells of chorionic villi but virtually absent from syncytiotrophoblast. In chorionic villi after RU486 administration in vivo, there were no obvious differences in prostaglandin dehydrogenase distribution or reactivity in the majority of cases.

show abstract

Progesterone and Estrogen Control of Uterine Prostaglandin Dehydrogenase Activity During Deciduomal Growth

Cited by 43 publications

References 0 publications

Local Modulation by 11 -Hydroxysteroid Dehydrogenase of Glucocorticoid Effects on the Activity of 15-Hydroxyprostaglandin Dehydrogenase in Human Chorion and Placental Trophoblast Cells

Local Modulation by 11 -Hydroxysteroid Dehydrogenase of Glucocorticoid Effects on the Activity of 15-Hydroxyprostaglandin Dehydrogenase in Human Chorion and Placental Trophoblast Cells

Altered white matter microarchitecture in the cingulum bundle in women with primary dysmenorrhea: A tract-based analysis study

The effects of mifepristone (RU486) on prostaglandin dehydrogenase in decidual and chorionic tissue in early pregnancy

Contact Info

Product

Resources

About