Oxytocin-stimulated phosphoinositide hydrolysis and prostaglandin F2α secretion by luminal epithelial, glandular epithelial and stromal cells from pig endometrium. II. Responses of cyclic, pregnant and pseudopregnant pigs on Days 12 and 1

2000 ◽  
Vol 12 (4) ◽  
pp. 157 ◽  
Author(s):  
Mehmet Uzumcu ◽  
Kevin G. Carnahan ◽  
Gheorghe T. Braileanu ◽  
Mark A. Mirando
Keyword(s):  
Epithelial Cells ◽  
Early Pregnancy ◽  
Stromal Cells ◽  
Prostaglandin F2α ◽  
Secretory Response ◽  
Reproductive Status ◽  
Phosphoinositide Hydrolysis ◽  
Pregnancy Recognition ◽  
Luminal Epithelial Cells

In pigs, the exact mechanism for the shift in endometrial PGF 2α secretion from an endocrine to an exocrine mode during pregnancy recognition is not known. The objective of this study was to examine whether this shift involved a change in the responsiveness of luminal epithelial, glandular epithelial and stromal cells to 0 or 100 nM oxytocin. Luminal epithelial cells, glandular epithelial cells and stromal cells were isolated from cyclic, pregnant or oestrogen-induced pseudopregnant gilts on Day 12 (Experiment 1) or Day 16 (Experiment 2) post oestrus (oestrus = Day 0). For cells obtained on Day 12, oxytocin stimulated PGF2α secretion by stromal cells (P<0.01) similarly for each reproductive status, whereas oxytocin stimulated PGF 2α secretion from luminal and glandular epithelial cells (P<0.05) from pregnant and pseudopregnant gilts but not from cyclic gilts. For both concentrations of oxytocin, mean PGF2α secretion was less (P<0.05) from stromal cells of pregnant than cyclic gilts. For cells obtained on Day 16, oxytocin stimulated PGF 2α release from stromal cells of cyclic gilts but not from stromal cells of pregnant gilts. Mean PGF 2α secretion also was less (P<0.05) from stromal cells of pregnant gilts than cyclic gilts. Oxytocin tended to stimulate PGF 2α release (P<0.07) from glandular epithelial cells of cyclic but not pregnant or pseudopregnant gilts. Luminal epithelial cells from all reproductive statuses were similarly unresponsive to oxytocin. In conclusion, the increased PGF2α secretory response to oxytocin of luminal and glandular epithelial cells from pregnant gilts on Day 12, combined with the decreased response of stromal cells from pregnant gilts on Days 12 and 16, may contribute, in part, to the shift in endometrial PGF2α secretion from an endocrine to an exocrine direction during early pregnancy in pigs.

Effect of ovarian steroids on basal and oxytocin-induced prostaglandin F2α secretion from pig endometrial cells

2003 ◽  
Vol 15 (4) ◽  
pp. 197 ◽  
Author(s):  
Jianbo Hu ◽  
Gheorghe T. Braileanu ◽  
Mark A. Mirando
Keyword(s):  
Epithelial Cells ◽  
Stromal Cells ◽  
Chronic Treatment ◽  
Prostaglandin F2α ◽  
Exocrine Secretion ◽  
Apical Surface ◽  
Stimulatory Action ◽  
Endometrial Cells ◽  
Oestradiol Treatment ◽  
Luminal Epithelial Cells

These studies were undertaken to determine how treatment with 100 nM progesterone and/or 10 nM oestradiol-17β acutely (3 h; Experiment 1) or chronically (72 h; Experiments 2–4) influenced basal and oxytocin (OT)-stimulated prostaglandin (PG) F2α secretion, in enriched cultures of pig endometrial luminal epithelial, glandular epithelial and stromal cells obtained on Day 16 (Experiments 1, 2 and 4) or Day 12 (Experiment 3) after oestrus. In Experiment 1, acute treatment with progesterone stimulated PGF2α secretion from each cell type on Day 16, whereas acute oestradiol treatment inhibited the stimulatory action of progesterone on PGF2α secretion only in glandular epithelial cells. In Experiment 2, OT stimulated phospholipase (PL) C activity in luminal epithelial cells on Day 16 only in the presence of chronic oestradiol treatment. For glandular epithelial cells on Day 16, OT stimulated PLC activity only in the presence of chronic treatment with steroid. In stromal cells on Day 16, OT stimulated PLC activity in the absence of steroids and the response to OT was further enhanced by oestradiol. In the absence of chronic treatment with steroid, OT did not stimulate PGF2α secretion from luminal epithelial cells, but oestradiol induced a response to OT. For glandular epithelial cells, OT-induced PGF2α secretion was not altered by steroids, whereas the stimulatory response to OT was inhibited by oestradiol or progesterone in stromal cells. For endometrial cells obtained on Day 12 after oestrus in Experiment 3, OT only stimulated PGF2α release from glandular epithelial and stromal cells. For luminal epithelial cells obtained on Day 16 after oestrus and cultured under polarizing conditions in Experiment 4, secretion of PGF2α occurred preferentially from the basolateral surface and was stimulated by OT more from the basolateral surface than from the apical surface. Oxytocin-induced PGF2α secretion from the apical surface was enhanced by chronic treatment with oestradiol, whereas that from the basolateral surface was enhanced by chronic treatment with progesterone. In summary, oestradiol enhanced OT-induced PGF2α secretion from the apical surface of luminal epithelial cells and reduced the response of stromal cells to OT, actions that may contribute to the reorientation of PGF2α from endocrine secretion (i.e. towards the uterine vasculature) to exocrine secretion (i.e. towards the uterine lumen) during pregnancy recognition in pigs.

Blastocyst-induced ATP release from luminal epithelial cells initiates decidualization through the P2Y2 receptor in mice

2020 ◽  
Vol 13 (646) ◽  
pp. eaba3396
Author(s):  
Xiao-Wei Gu ◽  
Zi-Cong Chen ◽  
Zhen-Shan Yang ◽  
Yan Yang ◽  
Ya-Ping Yan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Stromal Cells ◽  
Embryo Implantation ◽  
Atp Release ◽  
Sterile Inflammation ◽  
Short Exposure ◽  
Uterine Epithelial Cells ◽  
High Concentrations ◽  
Implantation Period ◽  
Luminal Epithelial Cells

Embryo implantation involves a sterile inflammatory reaction that is required for the invasion of the blastocyst into the decidua. Adenosine triphosphate (ATP) released from stressed or injured cells acts as an important signaling molecule to regulate many key physiological events, including sterile inflammation. We found that the amount of ATP in the uterine luminal fluid of mice increased during the peri-implantation period, and this depended on the presence of an embryo. We further showed that the release of ATP from receptive epithelial cells was likely stimulated by lactate released from the blastocyst through connexin hemichannels. The ATP receptor P2y2 was present on uterine epithelial cells during the preimplantation period and increased in the stromal cells during the time at which decidualization began. Pharmacological inhibition of P2y2 compromised decidualization and implantation. ATP-P2y2 signaling stimulated the phosphorylation of Stat3 in uterine luminal epithelial cells and the expression of early growth response 1 (Egr1) and prostaglandin-endoperoxide synthase 2 (Ptgs2, also known as Cox-2), all of which are required for decidualization and/or implantation, in stromal cells. Short exposure to high concentrations of ATP promoted decidualization of primary stromal cells, but longer exposures or lower ATP concentrations did not. The expression of genes encoding ATP-degrading ectonucleotidases increased in the decidua during the peri-implantation period, suggesting that they may limit the duration of the ATP signal. Together, our results indicate that the blastocyst-induced release of ATP from uterine epithelial cells during the peri-implantation period may be important for the initiation of stromal cell decidualization.

Functional Roles of Eph A-Ephrin A1 System in Endometrial Luminal Epithelial Cells During Early Pregnancy

2016 ◽  
Vol 232 (6) ◽  
pp. 1527-1538 ◽  
Author(s):  
Whasun Lim ◽  
Hyocheol Bae ◽  
Fuller W. Bazer ◽  
Gwonhwa Song
Keyword(s):  
Epithelial Cells ◽  
Early Pregnancy ◽  
Functional Roles ◽  
Luminal Epithelial Cells

scholarly journals Effect of LH on prostaglandin F2α and prostaglandin E2 secretion by cultured porcine endometrial cells

Reproduction ◽  
2005 ◽  
Vol 130 (1) ◽  
pp. 105-112 ◽  
Author(s):  
Agnieszka Blitek ◽  
Adam J Ziecik
Keyword(s):  
Epithelial Cells ◽  
Prostaglandin E2 ◽  
Stromal Cells ◽  
Prostaglandin F2α ◽  
Cell Types ◽  
Oestrous Cycle ◽  
Time Dependent ◽  
Dependent Effect ◽  
Endometrial Cells ◽  
Time Dependent Effect

LH appears to be a potent stimulator of the release of endometrial prostaglandins (PGs) in the pig. The aim of the present studies was to examine the effect of LH on PGF2αand PGE2secretion by cultured porcine endometrial cells on days 10–12 and 14–16 of the oestrous cycle and to compare its action with oxytocin. A time-dependent effect of LH (10 ng/ml) on PGF2αrelease from luminal epithelial and stromal cells on days 10–12 was observed (experiment 1). The highest increase in PGF2αsecretion in response to LH was detected in stromal cells after 6 h of incubation (P< 0.001). Epithelial cells responded to LH after a longer exposure time (P< 0.01). A concentration-dependent effect of LH (0.1–100 ng/ml) on PGF2αrelease from stromal cells was examined after 6 h and from epithelial cells after 12 h (experiment 2). Effective concentrations of LH were 10 and 100 ng/ml. LH (10 ng/ml) and oxytocin (100 nmol/l) affected PGF2αand PGE2secretion from endometrial cells on days 10–12 and 14–16 of the oestrous cycle (experiment 3). LH stimulated PGF2αsecretion from both cell types and its action was more potent on days 10–12. LH induced PGE2release, especially in epithelial cells on days 14–16. A stimulatory effect of oxytocin on PGF2αwas confirmed in stromal cells, but this hormone was also shown to enhance PGE2output. These results indicated that LH, like oxytocin, a very effective stimulator of PGF2αrelease, could play an important role in the induction of luteolysis.

scholarly journals Oxytocin and tumor necrosis factor α stimulate expression of prostaglandin E2 synthase and secretion of prostaglandin E2 by luminal epithelial cells of the porcine endometrium during early pregnancy

Reproduction ◽  
2010 ◽  
Vol 140 (4) ◽  
pp. 613-622 ◽  
Author(s):  
Agnieszka Waclawik ◽  
Agnieszka Blitek ◽  
Adam J Ziecik
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Prostaglandin E2 ◽  
Estrous Cycle ◽  
Early Pregnancy ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Luminal Epithelial Cells ◽  
Necrosis Factor

Oxytocin (OXT) and tumor necrosis factor α (TNF) have been implicated in the control of luteolysis by stimulating endometrial secretion of luteolytic prostaglandin F2α(PGF2α). Nevertheless, OXT concentration in porcine uterine lumen increases markedly on days 11–12 of pregnancy, and TNF is expressed in endometrium during pregnancy. The objective of the study was to determine the effect of OXT and TNF on expression of the enzymes involved in PG synthesis: PG-endoperoxide synthase 2 (PTGS2), PGE2synthase (mPGES-1) and PGF synthase, and PGE2receptor (PTGER2), as well as on PG secretion by endometrial luminal epithelial cells (LECs) on days 11–12 of the estrous cycle and pregnancy. LECs isolated from gilts on days 11–12 of the estrous cycle (n=8) and pregnancy (n=7) were treated with OXT (100 nmol/l) and TNF (0.6 nmol/l) for 24 h. OXT increasedPTGS2mRNA and mPGES-1 protein contents, as well as PGE2secretion but only on days 11–12 of pregnancy. TNF stimulatedPTGS2andmPGES-1mRNA, as well as mPGES-1 protein expression and PGE2release on days 11–12 of pregnancy and the estrous cycle. In addition, expressions of PTGER2 and PTGER4 were determined in corpus luteum (CL). Abundance ofPTGER2mRNA and PTGER4 protein in CL was upregulated on day 14 of pregnancy versus day 14 of the estrous cycle. This study indicates that TNF and OXT regulate PGE2synthesis in LECs during early pregnancy. PGE2secreted by LECs, after reaching ovaries, could have a luteoprotective effect through luteal PTGER2 and PTGER4, or may directly promote uterine function and conceptus development.

scholarly journals Expression and Function of Toll-Like Receptor 4 in the Endometrial Cells of the Uterus

Endocrinology ◽  
2006 ◽  
Vol 147 (1) ◽  
pp. 562-570 ◽  
Author(s):  
Shan Herath ◽  
Deborah P. Fischer ◽  
Dirk Werling ◽  
Erin J. Williams ◽  
Sonia T. Lilly ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Stromal Cells ◽  
Prostaglandin F2α ◽  
Endocrine Function ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Endometrial Cells ◽  
E Coli ◽  
Female Sex Hormones ◽  
And Function

Prostaglandins have a central role in many endocrine functions in mammals, including regulation of the life span of the corpus luteum by prostaglandin F2α (PGF) and prostaglandin E2 (PGE), which are secreted by the uterine endometrium. However, the uterus is readily infected with bacteria such as Escherichia coli, which disrupt luteolysis. Immune cells detect E. coli by Toll-like receptor 4 (TLR4) binding its pathogenic ligand, lipopolysaccharide (LPS), although signaling requires accessory molecules such as CD14. The objective of this study was to determine the effect of E. coli or LPS on the function of bovine endometrial cells, and whether purified populations of epithelial and stromal cells express the molecules involved in LPS recognition. In addition, because the female sex hormones estradiol and progesterone modify the risk of uterine infection, their effect on the LPS response was investigated. Endometrial explants produced prostaglandins in response to LPS, with an increased ratio of PGE to PGF. Addition of LPS or E. coli to stromal and epithelial cells stimulated production of PGE and PGF and increased their cyclooxygenase 2 mRNA expression. The production of prostaglandins was abrogated by an LPS antagonist. In addition, estradiol and progesterone inhibited the production of PGE and PGF in response to LPS, indicating a role for steroid hormones in the response to bacterial infection. For the first time, Toll-like receptor 4 mRNA and CD14 mRNA and protein were detected in bovine endometrial stromal and epithelial cells by RT-PCR and flow cytometry. In conclusion, epithelial and stromal cells detect and respond to bacteria, which modulate their endocrine function.

Localization of neutral endopeptidase in the ovine uterus and conceptus during the oestrous cycle and early pregnancy

1995 ◽  
Vol 7 (1) ◽  
pp. 27 ◽  
Author(s):  
SC Riley ◽  
E Wong ◽  
JK Findlay ◽  
LA Salamonsen
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Smooth Muscle Cells ◽  
Early Pregnancy ◽  
Stromal Cells ◽  
Immunohistochemical Staining ◽  
Muscle Cells ◽  
Neutral Endopeptidase ◽  
Oestrous Cycle ◽  
Ovine Uterus

Neutral endopeptidase (NEP; EC 3.4.24.11), an enzyme which metabolizes several peptides (including oxytocin and endothelins) implicated in the control of uterine function, was found to be localized in the ovine uterus throughout the oestrous cycle and in the uterus and conceptus during early pregnancy, using immunohistochemical techniques. Positive NEP immunoreactivity was found in the endometrium principally in stromal cells, in the vasculature in endothelial and vascular smooth muscle cells, and also weakly in some glandular epithelial cells. In a layer of stromal fibroblasts several cells in thickness underlying the luminal epithelium, staining was much weaker than that in the deeper stromal cells throughout the period examined. NEP staining was also present in smooth muscle cells of the myometrium at all times, and was most intense in the layer of cells adjacent to the endometrium. In the conceptus, NEP immunohistochemical staining was found in uninucleate cells, but not in binucleate trophoblast cells, in epithelial cells of the allantois and amnion, and in the heart and brain of the Day-20 embryo. In ovariectomized ewes treated with oestrogen or progesterone separately or remaining untreated, immunohistochemical staining of NEP was stronger when compared with intact ewes, in caruncular and intercaruncular stroma and epithelia, in glands, in the vasculature and in myometrium. The staining was less intense in all cell types in ewes receiving oestrogen plus progesterone. The expression of NEP and its specific regionalization within the uterus indicate a mechanism by which the availability of biologically important peptides involved in the regulation of the oestrous cycle and implantation, including oxytocin and endothelin, can be controlled by regulation of their metabolism.

scholarly journals Bacterial Lipopolysaccharide Induces an Endocrine Switch from Prostaglandin F2α to Prostaglandin E2 in Bovine Endometrium

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1912-1920 ◽  
Author(s):  
Shan Herath ◽  
Sonia T. Lilly ◽  
Deborah P. Fischer ◽  
Erin J. Williams ◽  
Hilary Dobson ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Prostaglandin E2 ◽  
Stromal Cells ◽  
Inflammatory Responses ◽  
Prostaglandin F2α ◽  
Uterine Disease ◽  
Group Vi ◽  
Endometrial Cells ◽  
Escherichia Coli Infection ◽  
Arachadonic Acid

Escherichia coli infection of the endometrium causes uterine disease after parturition and is associated with prolonged luteal phases of the ovarian cycle in cattle. Termination of the luteal phase is initiated by prostaglandin F2α (PGF) from oxytocin-stimulated endometrial epithelial cells. Compared with normal animals, the peripheral plasma of animals with E. coli infection of the endometrium had higher concentrations of lipopolysaccharide (LPS) and prostaglandin E2 (PGE) but not PGF. Endometrial explants accumulated predominantly PGE in the culture medium in response to LPS, and this effect was not reversed by oxytocin. Endometrial cells expressed the Toll-like receptor 4/CD14/MD-2 receptor complex necessary to detect LPS. Epithelial and stromal cells treated with LPS had higher steady-state media concentrations of PGE rather than PGF. Arachadonic acid is liberated from cell membranes by phospholipase 2 (PLA2) enzymes and converted to prostaglandins by synthase enzymes. Treatment of epithelial and stromal cells with LPS did not change the levels of PGE or PGF synthase enzymes. However, LPS stimulated increased levels of PLA2 group VI but not PLA2 group IV C immunoreactive protein in epithelial cells. Endometrial cells expressed the E prostanoid 2 and E prostanoid 4 receptors necessary to respond to PGE, which regulates inflammation as well as being luteotropic. In conclusion, LPS detection by endometrial cells stimulated the accumulation of PGE rather than PGF, providing a mechanism to explain prolonged luteal phases in animals with uterine disease, and this PGE may also be important for regulating inflammatory responses in the endometrium.

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