Differential expression and regulation of prostaglandin transporter and metabolic enzymes in mouse uterus during blastocyst implantation

Gao, Fei; Wei, Lei; Diao, Honglu; Hu, Shijun; Luan, Liming; Yang, Zeng‐Ming

doi:10.1016/j.fertnstert.2007.02.054

Cited by 11 publications

(9 citation statements)

References 46 publications

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“…of LPS on day 7 of gestation produced complete embryonic resorption at 24 h. We have found that after LPS administration, HPGD protein is expressed predominantly in the uterus, while in the decidua, the expression is almost undetectable. This result agrees with Gao et al (2007) who detected Hpgd mRNA and protein expression in the mouse uterus during embryo implantation. For this reason, we have focused on studying the modulation of 15-PGDH in the uterus.…”

Section: Discussionsupporting

confidence: 92%

“…Despite the physiological importance of 15-PGDH, little is understood about the mechanisms involved in regulating its expression. Expression and activity of 15-PGDH have been demonstrated in reproductive tissues of different species (Casey et al 1980, Kankofer 1999, Gao et al 2007. LPS treatment decreases activity of 15-PGDH in mouse and human fetal membranes at term (Brown et al 1998, Wang & Hirsch 2003 and alters Hpgd mRNA and protein levels in mouse and rat lung during sepsis (Hahn et al 1998, Ivanov & Romanovsky 2004).…”

Section: Introductionmentioning

confidence: 99%

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Lipopolysaccharide-induced murine embryonic resorption involves nitric oxide-mediated inhibition of the NAD+-dependent 15-hydroxyprostaglandin dehydrogenase

Aisemberg¹,

Bariani²,

Vercelli³

et al. 2012

Reproduction

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The initial inactivation of prostaglandins (PGs) is mediated by 15-hydroxyprostaglandin dehydrogenase (15-PGDH). PGs are potent mediators of several biological processes, including inflammation and reproduction. In uterus, PGs play a key role in infectioninduced pregnancy loss, in which concentration of this mediator increased. This process is accompanied with the induction of nitric oxide synthase expression and a marked increase in uterine levels of nitric oxide. There is no information concerning nitric oxide contribution to potential changes in PG catabolism, but experimental evidence suggests that nitric oxide modulates PG pathways. The specific objectives of the study were to evaluate the protein expression of HPGD (15-PGDH) and to characterize the nitric oxide-dependent regulation of this enzyme in a model of lipopolysaccharide (LPS)-induced embryonic resorption. Results show that LPS decreased HPGD protein expression and augmented PGE synthase activity; therefore, PGE 2 levels increased in uterus in this inflammatory condition. Just as LPS, the treatment with a nitric oxide donor diminished HPGD protein expression in uterine tissue. In contrast, the inhibition of nitric oxide synthesis both in control and in LPS-treated mice increased 15-PGDH levels. Also, we have found that this enzyme and PGE 2 levels are not modulated by peroxynitrite, an oxidant agent derived from nitric oxide. This study suggests that LPS and nitric oxide promote a decrease in the ability of the uterus for PG catabolism during bacterially triggered pregnancy loss in mice.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide-induced murine embryonic resorption involves nitric oxide-mediated inhibition of the NAD+-dependent 15-hydroxyprostaglandin dehydrogenase

Aisemberg¹,

Bariani²,

Vercelli³

et al. 2012

Reproduction

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“…These findings were somewhat different from the results shown in other species. In mice, Cbr1 mRNA is localized to uterine GE until Day 4 of pregnancy but not after embryo implantation [19], and endometrial HPGD expression is detected in uterine GE in cattle [20] and placental trophoblast in humans [42], suggesting that the mechanism to regulate PGE 2 and PGF 2a metabolism at the maternal-fetal interface during pregnancy may be species specific.…”

Section: Discussionmentioning

confidence: 99%

“…PGs are catabolized mainly by hydroxyprostaglandin dehydrogenase (HPGD) to terminate their action [17]. Expression of HPGD in the uterine endometrium has been reported for humans [18], mice [19], and cows [20] but not pigs. Expression of PTGS1, PTGS2, PTGES, and CBR1 has been reported in the uterine endometrium during early pregnancy in pigs [9,[21][22][23], but expression of these during the later stage of pregnancy and other enzymes involved in PGE 2 and PGF 2a synthesis and metabolism during pregnancy has not been completely studied in pigs.…”

Section: Introductionmentioning

confidence: 99%

Comprehensive Analysis of Prostaglandin Metabolic Enzyme Expression During Pregnancy and the Characterization of AKR1B1 as a Prostaglandin F Synthase at the Maternal-Conceptus Interface in Pigs1

Seo

Choi

Shim

et al. 2014

Biology of Reproduction

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Prostaglandins (PGs) are important lipid mediators regulating various reproductive processes in many species. In pigs, the expression pattern of PGE2 and PGF2α metabolic enzymes and the regulatory mechanism controlling PGE2 and PGF2α levels in the uterus during pregnancy are not completely understood. This study determined endometrial expression of the genes (PLA2G4A, PTGS1, PTGS2, PTGES, PTGES2, PTGES3, AKR1B1, CBR1, and HPGD) involved in PGE2 and PGF2α metabolism during the estrous cycle and pregnancy and measured levels of PGE2 and PGF2α in uterine endometrial tissues and uterine flushings at the time of conceptus implantation in pigs. Except PTGES3, expression of the genes studied changed in a pregnancy-stage-specific manner, and localization of PTGES, AKR1B1, CBR1, and HPGD mRNAs were cell-type specific in the uterine endometrium. Levels of both PGE2 and PGF2α in uterine endometrial tissues and uterine lumen were higher on Day 12 of pregnancy than those of the estrous cycle and affected by different morphology of spherical and filamentous conceptuses. Furthermore, we determined that endometrial expression of AKR1B1, known to encode a PGF2α synthase in other species, was increased by estrogen and interleukin-1beta and that AKR1B1 exhibited PGF2α synthase activity in the porcine uterine endometrium. These results in pigs indicate that the PGE2 and PGF2α metabolic enzymes are expressed stage specifically in the endometrium during pregnancy and regulate the abundance of PGE2 and PGF2α in the uterus at the time of implantation and that AKR1B1 may act as a major PGF synthase in the endometrium during early pregnancy.

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“…Estradiol-17b (E 2 , Sigma) and progesterone (P 4 , Sigma) were dissolved in sesame oil and injected S.C. Ovariectomized mice were injected with estradiol-17b (100 ng/mouse), progesterone (2 mg/mouse), or a combination of the same doses of progesterone and estradiol-17b (E 2 ? P 4 ), respectively (Gao et al 2007). The mice were sacrificed for uterus collection at 2, 4, 6, 12 and 24 h after steroid hormone treatments.…”

Section: Animals and Treatmentsmentioning

confidence: 97%

Hormonal regulation of uterine natural killer cells in mouse preimplantation uterus

Kuang

Peng

et al. 2010

J Mol Hist

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Uterine Natural Killer (uNK) cells are the most abundant lymphocyte population recruited in the uteri during murine and human pregnancy. Previous investigation on uNK cells during mouse pregnancy focused more on its accumulation in postimplantation periods, which were believed to play important roles in regulating trophoblast invasion and angiogenesis towards successful placentation. However, by using recently developed methods of Dolichos biflorus agglutinin (DBA) lectin, a closer examination during mouse preimplantation revealed that there were also dynamic regulations of uNK cell, suggesting a major regulation by steroid hormones. Here we provide a detailed examination of uNK cells distribution during mouse early pregnancy by DBA lectin reactivity, with emphasis on preimplantation period and its hormonal regulation profiles. Our results showed that uNK precursor cells or its cell membrane specific components could be recruited in the uterus by estrogen or/and progesterone, and the effects could be completely abolished by specific antagonists of their nuclear receptors (estrogen and progesterone receptor). These results suggested that the preimplantation uterus, through concerted hormone regulation, could recruit uNK precursor cell or its specific cellular component, which might be conducive for uterine receptivity and further uNK construction/function during postimplantation.

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Differential expression and regulation of prostaglandin transporter and metabolic enzymes in mouse uterus during blastocyst implantation

Cited by 11 publications

References 46 publications

Lipopolysaccharide-induced murine embryonic resorption involves nitric oxide-mediated inhibition of the NAD+-dependent 15-hydroxyprostaglandin dehydrogenase

Lipopolysaccharide-induced murine embryonic resorption involves nitric oxide-mediated inhibition of the NAD+-dependent 15-hydroxyprostaglandin dehydrogenase

Comprehensive Analysis of Prostaglandin Metabolic Enzyme Expression During Pregnancy and the Characterization of AKR1B1 as a Prostaglandin F Synthase at the Maternal-Conceptus Interface in Pigs1

Hormonal regulation of uterine natural killer cells in mouse preimplantation uterus

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