Human Uterine Epithelial Cells: Influence of culture conditions and stromal cells on epithelial cell transepithelial cell resistance

1999 ◽  
pp. 366-378 ◽  
Author(s):  
John V. Fahey ◽  
Charu Kaushic ◽  
Charles R. Wira
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Stromal Cells ◽  
Culture Conditions ◽  
Cell Resistance ◽  
Uterine Epithelial Cells

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.

scholarly journals Polarised bovine endometrial epithelial cells vectorially secrete prostaglandins and chemotactic factors under physiological and pathological conditions

Reproduction ◽  
2013 ◽  
Vol 145 (1) ◽  
pp. 57-72 ◽  
Author(s):  
Siân B MacKintosh ◽  
Hans-Joachim Schuberth ◽  
Laura L Healy ◽  
I Martin Sheldon
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Bacterial Infection ◽  
Stromal Cells ◽  
Neutrophil Migration ◽  
Response To Treatment ◽  
Prostaglandin E ◽  
Prostaglandin F ◽  
Chemotactic Factors ◽  
Endometrial Epithelial Cells

Epithelial cells of the endometrium secrete prostaglandins to regulate the bovine oestrous cycle and form a functional barrier to microbes. However, bacterial infection of the endometrium commonly causes infertility in dairy cattle by disrupting endometrial physiology. Epithelial cell cultures are used to study the mechanisms of physiology and pathology, but 2D cultures may not reflect the 3D complexity of the epithelium. In this study, a polarised epithelial cell transwell culture was developed, using transepithelial resistance (TER), to monitor epithelial integrity. Polarised epithelial cells were treated with oxytocin and arachidonic acid to test physiological function and with lipopolysaccharide (LPS) to mimic bacterial infection. Supernatants were analysed for prostaglandin E2(PGE), prostaglandin F2α, the chemokine interleukin-8 (IL8) and the ability of supernatants to induce neutrophil migration. Confluent epithelial cells established polarity when TER was >1800 Ωcm2and predominantly released prostaglandins basolaterally. In contrast, IL8 from epithelial cells accumulated apically and the supernatants were highly chemotactic for neutrophils. The striking exception was when the epithelial cells were treated with LPS in the apical or basolateral compartment independently, which led to the release of IL8 towards the treated compartment. Although stromal cells also accumulated PGE and IL8 in response to treatment, co-culture of stromal cells in the well below polarised epithelial cells did not influence cellular responses. In conclusion, polarised endometrial epithelial cells vectorially released prostaglandins and chemokines to reflect their respective mechanistic roles in physiology and pathology.

412. The role of macrophages in regulating uterine epithelial cell proliferation

2008 ◽  
Vol 20 (9) ◽  
pp. 92
Author(s):  
A. S. Care ◽  
W. V. Ingman ◽  
M. J. Jasper ◽  
SA Robertson
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Diphtheria Toxin ◽  
Functional Markers ◽  
Epithelial Cell Proliferation ◽  
Uterine Epithelial Cells ◽  
Uterine Epithelial Cell ◽  
Macrophage Depletion ◽  
Embryo Attachment

During the oestrous cycle, uterine epithelial cells respond to ovarian steroid hormones by producing an array of cytokines and chemokines that cause macrophage recruitment into the uterus and regulate macrophage activation phenotype. In turn, growth factors and cytokines synthesised by macrophages potentially impact epithelial cell proliferation, secretory function and receptivity to embryo attachment. To investigate the hypothesis that uterine macrophages are essential contributors to the proliferation of uterine epithelial cells, we have used an ovariectomy and steroid replacement model in CD11b-DTR ‘Mac-terminator' mice. These mice are engineered for CD11b promoter-driven expression of the monkey diphtheria toxin (DT) receptor, allowing acute systemic ablation of macrophages by administration of human diphtheria toxin (DT). CD11b-DTR mice were ovariectomised, then 2–4 weeks later were primed with E 2, followed by administration of DT (25 ng/g, ip) to effect macrophage depletion, and BrDU to label proliferating cells. Control mice were given PBS instead of DT. Uterine tissues were stained with F4/80 to detect macrophages, and anti-BrDU to detect BrDU+ epithelial cell nuclei. DT treatment was associated with a depletion of >90% of F4/80+ uterine macrophages. However, the numbers of BrDU+ epithelial cells and the architecture of the luminal epithelial surface and abundance of epithelial glands were similar in control and DT-treated uterine tissues. These data suggest that resident macrophages may not be essential for oestrogen-driven uterine epithelial cell proliferation. In ongoing experiments we are assessing the effect of macrophage depletion on epithelial cell expression of functional markers including those involved in regulation of embryo attachment.

scholarly journals Deficiency of Reproductive Tract α(1,2)Fucosylated Glycans and Normal Fertility in Mice with Targeted Deletions of the FUT1 or FUT2 α(1,2)Fucosyltransferase Locus

2001 ◽  
Vol 21 (24) ◽  
pp. 8336-8345 ◽  
Author(s):  
Steven E. Domino ◽  
Liang Zhang ◽  
Patrick J. Gillespie ◽  
Thomas L. Saunders ◽  
John B. Lowe
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Reproductive Tract ◽  
Normal Development ◽  
Sperm Maturation ◽  
Male Reproductive Tract ◽  
Uterine Epithelial Cells ◽  
Uterine Epithelial Cell ◽  
Normal Fertility ◽  
Genes Encoding

ABSTRACT The fucose α(1→2) galactose β structure is expressed by uterine epithelial cells in the mouse and has been implicated in blastocyst adhesion events thought to be required for murine implantation. Fucα(1→2)Galβ moieties and cognate fucosyltransferases are also expressed by epithelial cells of the male reproductive tract and have been implicated in sperm maturation events that may contribute to fertilization. To determine directly if Fucα(1→2)Galβ moieties are required for fertility, we have generated strains of mice that are deficient in genes encoding FUT1 and FUT2, a pair of GDP-l-fucose:β(1→4)-d-galactosyl-R2-α-l-fucosyltransferase enzymes (EC 2.4.1.69 ) responsible for Fucα(1→2)Galβ synthesis and expression. FUT1 null mice and FUT2 null mice develop normally and exhibit no gross phenotypic abnormalities. The Fucα(1→2)Galβ epitope is absent from the uterine epithelia of FUT2 null mice and from the epithelia of the epididymis of FUT1 null mice. Fully normal fertility is observed in FUT1 null intercrosses and in FUT2 null intercrosses. These observations indicate that Fucα(1→2)Galβ moieties are not essential to blastocyst-uterine epithelial cell interactions required for implantation and are not required for sperm maturation events that permit fertilization and that neither the FUT loci nor their cognate fucosylated glycans are essential to normal development.

111. LIF REGULATION OF EPITHELIAL CELL FUCOSYLTRANSFERASE EXPRESSION IN MOUSE ENDOMETRIUM DURING EARLY PREGNANCY

2009 ◽  
Vol 21 (9) ◽  
pp. 30
Author(s):  
M. J. Jasper ◽  
A. Care ◽  
J. D. Aplin ◽  
S. A. Robertson
Keyword(s):  
Epithelial Cell ◽  
Epithelial Cells ◽  
Mrna Expression ◽  
Seminal Vesicle ◽  
Diphtheria Toxin ◽  
Embryo Implantation ◽  
Mouse Uterus ◽  
Uterine Epithelial Cells

Fucosyltransferase (FUT) enzymes are key regulators of glycosylated structures mediating embryo attachment to uterine epithelial cells at implantation. The identity of local regulatory signals is unknown. We have previously shown that macrophage co-culture significantly increases epithelial cell FUT2 and FUT4 mRNA expression in vitro, and the effect of co-culture is replicated with macrophage conditioned media. We aimed to define the identity of macrophage-secreted agents active in regulating FUT expression in mouse uterine epithelial cells, and to investigate the importance of macrophages for FUT expression in vivo. FUT1, FUT2, and FUT4 mRNAs were measured by qRT-PCR and data was normalised to β-actin mRNA in mouse uterine epithelial cells after culture with cytokines known to be secreted by macrophages. mRNA was also quantified in luminal epithelium laser-microdissected from mouse uterus on day 4 after mating with intact males or seminal vesicle deficient (SVX) males, to induce normal or depleted uterine macrophage populations respectively. Lectin staining on day 4 pc was quantified using ImageJ software in an alternate model of transient, systemic macrophage ablation following diphtheria toxin administration to CD11b-DTR transgenic mice. Epithelial FUT2 mRNA expression was specifically enhanced in vitro by addition of rLIF (2 ng/ml) (mean relative expression ± SEM, control 100 ± 5.6; rLIF 162.1 ± 11.5). Depletion of macrophages by mating with seminal vesicle deficient males reduced epithelial FUT2 mRNA expression on day 4 pc (intact 100 ± 9.1; SVX 73.5 ± 8.6). Depletion of macrophages in the CD11b-DTR mouse model caused a 30% reduction in the expression of the resulting glycoprotein epitope (α1,2 fucose) as observed by intensity of endometrial epithelial UEA-1 staining (control 100 ± 10; CD11b-DTR 72 ± 9) 24 hr post diphtheria toxin administration. In conclusion, these data demonstrate that endometrial epithelial FUT2 mRNA synthesis in preparation for embryo implantation is mediated via LIF and potentially other factors secreted from macrophages recruited during the inflammatory response to insemination. Uterine macrophage abundance and phenotype may thus be a determinant of receptivity to implantation.

Electron Microscopic Study of the Epithelium of the Seminal Vesicle of Aging Rats

1974 ◽  
Vol 32 ◽  
pp. 138-139
Author(s):  
V. F. Allison ◽  
G. C. Fink ◽  
G. W. Cearley
Keyword(s):  
Cell Growth ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Seminal Vesicle ◽  
Seminal Vesicles ◽  
Epithelial Layer ◽  
Epithelial Hyperplasia ◽  
Electron Microscopic ◽  
Aging Rats ◽  
Pseudostratified Epithelium

It is well known that epithelial hyperplasia (benign hypertrophy) is common in the aging prostate of dogs and man. In contrast, little evidence is available for abnormal epithelial cell growth in seminal vesicles of aging animals. Recently, enlarged seminal vesicles were reported in senescent mice, however, that enlargement resulted from increased storage of secretion in the lumen and occurred concomitant to epithelial hypoplasia in that species.The present study is concerned with electron microscopic observations of changes occurring in the pseudostratified epithelium of the seminal vescles of aging rats. Special attention is given to certain non-epithelial cells which have entered the epithelial layer.

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