The process of blastocyst implantation in mammals is remarkably variable, especially in the extent of trophoblast invasion of the endometrium. In most species studied, the earliest macroscopically identifiable sign of blastocyst implantation is an increase in endometrial vascular permeability in areas adjacent to the blastocysts. This is followed in species with invasive implantation by decidualization, again localized to areas adjacent to the blastocysts. In some species, the application of a stimulus to the endometrium can result in increased endometrial vascular permeability and decidualization. Based initially on studies utilizing inhibitors of prostaglandin (PG) synthesis and more recently on studies using the techniques of transgenics, considerable evidence has accumulated indicating that PGs have an important role in the early events of implantation and artificially induced decidualization. However, which PGs are involved remains controversial. There may be differences between species, and different PGs may be involved at different times.

/pdf/prostaglandins-and-the-initiation-of-blastocyst-implantation-3me97bctpw.pdf

Prostaglandins and the initiation of blastocyst implantation and decidualization.

Prokineticin 1 (PROK1) is a recently described protein with a wide range of functions including tissue-specific angiogenesis, modulation of inflammatory responses, and regulation of hematopoiesis. The objective of this study was to investigate the role of PROK1 and prokineticin receptor 1 (PROKR1) in human endometrium during early pregnancy. PROK1 and PROKR1 expression is significantly elevated in first-trimester decidua, compared with nonpregnant endometrium. Expression of PROK1 and PROKR1 was localized in glandular epithelial and various cellular compartments within the stroma. To investigate the signaling pathways and target genes activated by PROK1, we generated an endometrial epithelial cell line stably expressing PROKR1 (Ishikawa PROKR1 cells). PROK1-PROKR1 interaction induced inositol phosphate mobilization and sequential phosphorylation of c-Src, epidermal growth factor receptor, and ERK 1/2. Gene microarray analysis on RNA extracted from Ishikawa PROKR1 cells treated with 40 nm PROK1 for 8 h reve...

/pdf/prokineticin-1-signaling-and-gene-regulation-in-early-human-3ugwth3ct7.pdf

Prokineticin 1 Signaling and Gene Regulation in Early Human Pregnancy

Prostaglandins (PGs) play a pivotal role in luteolysis, maternal recognition of pregnancy, and implantation. In many species, including pigs, both conceptus (embryo and associated membranes) and endometrium synthesize PGE2, which may antagonize PGF2a by playing a luteotropic/antiluteolytic role. Previously, we have reported expression profiles of PG G/H synthases (PGHS-1 and PGHS-2), PGE synthase (mPGES-1), and PGF synthase (PGFS) in the endometrium of cyclic and pregnant pigs. In the present study, expression of abovementioned PG synthesis enzymes and PG 9-ketoreductase (CBR1), which converts PGE2 into PGF2a ,a nd the PGE2/PGF2a ratios were investigated in porcine peri- and post-implantation conceptuses. Furthermore, expression of CBR1 was examined in the endometrium. PGHS-2 and mPGES-1 were upregulated, and PGHS-1, PGFS, and CBR1 were downregulated in conceptuses during trophoblastic elongation. A second increase of mPGES-1 mRNA occurred after days 20‐21 of pregnancy. After initiation of implantation, expression of PGHS-1, PGFS, and CBR1 in conceptuses increased and remained higher until days 24‐25 of pregnancy. Comparison of the endometrial CBR1 protein expression in cyclic and pregnant gilts revealed upregulation on days 16‐17 of the cycle and downregulation on days 10‐11 of pregnancy. In conclusion, reciprocal expression of PGHS-2, mPGES-1, PGFS, and CBR1 in day 10‐13 conceptuses and decrease of endometrial CBR1 may be important in increasing the PGE2/PGF2a ratio during maternal recognition of pregnancy. This study indicates that PGE2 produced via PGHS-2 and mPGES-1 in conceptus may be involved in corpus luteum control. Moreover, high expression of conceptus PGHS-1, mPGES-1, PGFS, and CBR1 after initiation of implantation suggests their significant role in placentation.

/pdf/differential-expression-of-prostaglandin-pg-synthesis-1zoq0roivh.pdf

Differential expression of prostaglandin (PG) synthesis enzymes in conceptus during peri-implantation period and endometrial expression of carbonyl reductase/PG 9-ketoreductase in the pig

How endometrial secretomics can help in predicting implantation

BACKGROUND: The invasion of first trimester extravillous trophoblast (EVT) to decidua is an important event in placentation. Leukemia inhibitory factor (LIF) is an essential factor for mouse implantation, and it is reported that LIF may be involved in human first trimester EVT invasion. Prostaglandin E 2 (PGE 2 ) is also known as a critical factor for first trimester EVT invasion. In this study, we investigated the role of LIF in PGE 2 production and EVT invasion using a human first trimester EVT cell line, HTR-8/SVneo. METHODS and RESULTS: Co-stimulation with LIF and IL-1β induced higher amounts of PGE 2 production and further migration of HTR-8/SVneo cells compared with that by stimulation with LIF or IL-lp alone. Enhanced PGE 2 production was most probably due to the enhanced expression of cyclooxygenase-2 (COX-2) and microsomal PGE synthase-1 (mPGES-1). PGE 2 produced by HTR-8/SVneo cells promoted the migration of HTR-8/SVneo cells. A COX-2 inhibitor suppressed PGE 2 production and the migration of HTR-8/SVneo cells. Agonists to PGE 2 receptors, EP1, EP2 and EP4, promoted the migration of HTR-8/SVneo cells. Moreover, stimulation with LIF up-regulated EP1, EP2 and EP4 expression in HTR-8/SVneo cells. CONCLUSIONS: It is suggested that LIF participates in placentation through EVT invasion by up-regulating PGE 2 production and PGE 2 receptor expression in first trimester EVT.

/pdf/induction-of-prostaglandin-e2-production-by-leukemia-1szgymp7cu.pdf

Induction of prostaglandin E2 production by leukemia inhibitory factor promotes migration of first trimester extravillous trophoblast cell line, HTR-8/SVneo

Prostaglandin E2 is a product of induced prostaglandin-endoperoxide synthase 2 and microsomal-type prostaglandin E synthase at the implantation site of the hamster.

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Prostaglandin E2 is a product of induced prostaglandin-endoperoxide synthase 2 and microsomal-type prostaglandin E synthase at the implantation site of the hamster.