Prostaglandin-Metabolizing Enzymes During Pregnancy: Characterization of NAD<sup>+</sup>-Dependent Prostaglandin Dehydrogenase, Carbonyl Reductase, and Cytochrome P450-Dependent Prostaglandin Omega-Hydroxylase

Okita, Richard T.; Okita, Janice R.

doi:10.3109/10409239609106581

Cited by 64 publications

(25 citation statements)

References 108 publications

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“…Many factors, including drugs (Flower, 1974), proteinmodifying agents, zinc and copper metal ions (Sakuma et al, 1990(Sakuma et al, , 1996, hyperoxia (Parkes and Eling, 1975;Chaudhari et al, 1979;Vader et al, 1981;Pisarello et al, 1997), fatty acids, cAMP (Lennon et al, 1999), calcium, bacterial endotoxins (lipopolysaccharide) (Alam et al, 1973;Nakano and Prancan, 1973;Blackwell et al, 1976;Harper et al, 1980;Hahn et al, 1998), 1,25-dihydroxyvitamin D3 (Pichaud et al, 1997), vitamin E (Chan et al, 1980, thyroid hormones (Tai et al, 1974;Moore and Hoult, 1978), cytokines (Brown et al, 1998) and steroid hormones, have been implicated in the regulation of PGDH activity in a variety of species and types of cell (Nakano and Prancan, 1973;Andersen and Ramwell, 1974;Lee and Levine, 1975;Hansen, 1976;Tai and Hollander, 1976;Pace-Asciak and Smith, 1983;Krook et al, 1992;Okita and Okita, 1996). The 1.6 kb promoter region of the PGDH gene contains two TATA boxes and a number of potential regulatory elements, including Sp1, CRE, GRE, AP1, AP2, NF-IL6, C-MYC and a putative oestrogen receptor binding site (Matsuo et al, 1996(Matsuo et al, , 1997.…”

Section: Prostaglandin Metabolismmentioning

confidence: 99%

Prostaglandins and mechanisms of preterm birth

Challis¹,

Sloboda²,

Alfaidy³

et al. 2002

Reproduction

307

112

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Preterm birth (birth before week 37 of gestation) occurs in approximately 5-10% of all pregnancies. This value may be higher in certain population groups and has not decreased over the past 20-30 years. Although some preterm births may be elective, approximately 30% occur in association with an underlying infectious process, and about 50% are idiopathic preterm births of unknown cause. Preterm birth is associated with 70% of neonatal deaths, and up to 75% of neonatal morbidity. Infants born preterm have an increased incidence of blindness, deafness, cerebral palsy, neurological disorders and pulmonary disorders (Morrison, 1990;

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Section: Prostaglandin Metabolismmentioning

confidence: 99%

Prostaglandins and mechanisms of preterm birth

Challis¹,

Sloboda²,

Alfaidy³

et al. 2002

Reproduction

307

112

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“…Studies in mice with deletion of PGF receptor FP (Ptgfr -/-) show that PGF 2α acts on ovarian FP receptors to induce luteolysis, leading to the fall in P 4 levels required for triggering labor (44). PGE 2 and PGF 2α are primarily metabolized by 15-HPGD (45,46), and mice carrying 15-HPGD hypomorphic alleles show spontaneous preterm labor with increased levels of PGF 2α in the absence of luteolysis and P 4 withdrawal (47). We observed similar circulating levels of E 2 and P 4 in Trp53 loxP/loxP Pgr +/+ and Trp53 loxP/loxP Pgr Cre/+ dams without luteolysis on day 16 ( Figure 5, G-J), which suggests that the onset of preterm labor in Trp53 loxP/loxP Pgr Cre/+ mice is caused by direct contractile effects of higher COX2-derived PGF 2α levels in the uterus, not by early luteolysis.…”

Section: Trp53 Is Efficiently Deleted In Uteri Ofmentioning

confidence: 99%

Uterine-specific p53 deficiency confers premature uterine senescence and promotes preterm birth in mice

Hirota¹,

Daikoku²,

Tranguch³

et al. 2010

J. Clin. Invest.

212

248

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Many signaling pathways that contribute to tumorigenesis are also functional in pregnancy, although they are dysregulated in the former and tightly regulated in the latter. Transformation-related protein 53 (Trp53), which encodes p53, is a tumor suppressor gene whose mutation is strongly associated with cancer. However, its role in normal physiological processes, including female reproduction, is poorly understood. Mice that have a constitutive deletion of Trp53 exhibit widespread development of carcinogenesis at early reproductive ages, compromised spermatogenesis, and fetal exencephaly, rendering them less amenable to studying the role of p53 in reproduction. To overcome this obstacle, we generated mice that harbor a conditional deletion of uterine Trp53 and examined pregnancy outcome in females with this genotype. These mice had normal ovulation, fertilization, and implantation; however, postimplantation uterine decidual cells showed terminal differentiation and senescence-associated growth restriction with increased levels of phosphorylated Akt and p21, factors that are both known to participate in these processes in other systems. Strikingly, uterine deletion of Trp53 increased the incidence of preterm birth, a condition that was corrected by oral administration of the selective COX2 inhibitor celecoxib. We further generated evidence to suggest that deletion of uterine Trp53 induces preterm birth through a COX2/PGF synthase/PGF 2α pathway. Taken together, our observations underscore what we believe to be a new critical role of uterine p53 in parturition.

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“…However, less is known about how the degradation of prostaglandins may be regulated to achieve increased prostaglandin levels and parturition at term. 15-Hydroxyprostaglandin dehydrogenase (15-HPGD) is the principal enzyme responsible for the breakdown of PGF 2␣ as well as the less robustly expressed prostaglandin E 2 (PGE 2 ) (42,43). In humans, 15-HPGD mRNA decreases in chorion trophoblast cells in both term and preterm laboring women versus nonlaboring women (44,45).…”

Section: -Hydroxyprostaglandin Dehydrogenase Decreases At Term To Amentioning

confidence: 99%

Insights Into Parturition Biology From Genetically Altered Mice

Ratajczak

Muglia

2008

Pediatr Res

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ABSTRACT:With the growing frequency of preterm birth, increased effort has been made to elucidate the physiology of normal and aberrant parturition. As with many developmental processes, the study of genetically altered mice has led to an increased understanding of mechanisms controlling the maintenance and resolution of pregnancy. Studies in genetically altered mice have implicated critical roles for both prostaglandin synthesis and degradation in luteolysis and the progression of labor. The importance of local modulation of progesterone activity to cervical ripening has also been demonstrated. Although a decline in levels of serum progesterone is a part of normal labor initiation in mice but not humans, murine labor without progesterone withdrawal has been reported in some cases. These findings emphasize the importance of other components of the parturition cascade that are shared in mice and humans and highlights the importance of an increased understanding of the physiology of mouse parturition. (Pediatr Res 64: 581-589, 2008) P arturition is the culmination of mammalian reproduction, a task essential for survival of the species. After a period of uterine quiescence to allow fetal growth and development, changes occur in myometrial contractility that result in efficient expulsion of the fetus. These events have likely evolved to enhance survival of both the fetus and the mother. The nature of these pathways, however, is at best incompletely defined.Increased knowledge of the cascade of events that occur at parturition may lead to advances in combating preterm labor (PTL) or optimization of protocols for medically induced labor. As preterm birth is associated with both increased risk of neonatal mortality and chronic sequelae such as respiratory illness, cerebral palsy, and vision and hearing impairment, it is a major public health concern (1). In the United States, 12.7% of births are preterm (2). Although approximately 50% of preterm births are idiopathic (3), genetic factors seem to be important. Women whose mothers or sisters delivered preterm are at increased risk for premature labor (4,5), indicating a genetic component in the timing of labor. In addition, a study of a Utah population indicates greater genetic relatedness between families with preterm deliveries than control families (6). Because the population studied was descended from the people who established Mormonism in Utah and Mormons have low rates of substance abuse and sexually transmitted diseases, the population used in this study may represent individuals with few environmental risk factors for PTL (6). These studies highlight a role for genetic, and not just environmental factors in predisposition to PTL and serves as a call to researchers to identify and study genes important for parturition.The mouse is a useful research tool for dissecting genetic factors involved in developmental processes. Mice are tractable to genetic manipulation, resulting in an array of available and potential knockout and transgenic mice suitable for studying t...

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Prostaglandin-Metabolizing Enzymes During Pregnancy: Characterization of NAD⁺-Dependent Prostaglandin Dehydrogenase, Carbonyl Reductase, and Cytochrome P450-Dependent Prostaglandin Omega-Hydroxylase

Cited by 64 publications

References 108 publications

Prostaglandins and mechanisms of preterm birth

Prostaglandins and mechanisms of preterm birth

Uterine-specific p53 deficiency confers premature uterine senescence and promotes preterm birth in mice

Insights Into Parturition Biology From Genetically Altered Mice

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Prostaglandin-Metabolizing Enzymes During Pregnancy: Characterization of NAD+-Dependent Prostaglandin Dehydrogenase, Carbonyl Reductase, and Cytochrome P450-Dependent Prostaglandin Omega-Hydroxylase

Cited by 64 publications

References 108 publications

Prostaglandins and mechanisms of preterm birth

Prostaglandins and mechanisms of preterm birth

Uterine-specific p53 deficiency confers premature uterine senescence and promotes preterm birth in mice

Insights Into Parturition Biology From Genetically Altered Mice

Contact Info

Product

Resources

About

Prostaglandin-Metabolizing Enzymes During Pregnancy: Characterization of NAD⁺-Dependent Prostaglandin Dehydrogenase, Carbonyl Reductase, and Cytochrome P450-Dependent Prostaglandin Omega-Hydroxylase