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

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.

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.

237. Aquaporins in rat uterine epithelial cells during early pregnancy and in response to progesterone

2005 ◽  
Vol 17 (9) ◽  
pp. 93
Author(s):  
L. A. Lindsay ◽  
C. R. Murphy
Keyword(s):  
Plasma Membrane ◽  
Epithelial Cells ◽  
Early Pregnancy ◽  
Water Movement ◽  
Immunogold Electron Microscopy ◽  
Apical Plasma Membrane ◽  
Uterine Lumen ◽  
Epithelial Barriers ◽  
Luminal Epithelial Cells ◽  
Ovariectomised Rats

Implantation of the rat blastocyst is a highly regulated process, involving transformation of the uterine environment into one which is receptive to an implanting blastocyst. At the time of implantation, in response to progesterone, there is a dramatic decrease in the amount of uterine luminal fluid leading to close apposition between the luminal epithelium and trophoblastic cells. The rat blastocyst also always implants at the antimesometrial pole of the uterine lumen and currently mechanisms regulating this process are unknown. Aquaporins, a family of transmembrane water channels, are involved in the regulation of water movement across epithelial barriers. We investigated several aquaporins in the rat uterus during early pregnancy using reverse transcriptase PCR. Immunofluorescence and immunogold electron microscopy techniques were then used to investigate the localisation of particular aquaporins including AQP5 in the uterine epithelium during early pregnancy and in ovariectomised rats treated with progesterone. There was an increase in AQP5 molecules in the apical plasma membrane of luminal epithelial cells at the time of implantation, with a greater increase at the mesometrial compared to antimesometrial pole. A similar result was seen in luminal epithelial cells from ovariectomised rats treated with progesterone, however there was no differential concentration between mesometrial and antimesometrial poles, as there was during early pregnancy. It is suggested that the increase in AQP5 protein expression in the apical plasma membrane of luminal epithelial cells is involved in reabsorption of luminal fluid at the time of implantation. Furthermore, the differential concentration of AQP5 on luminal epithelial cells at the time of implantation could lead to the establishment of a fluid gradient within the uterine lumen and hence lead to the asymmetrical implantation position of the rat blastocyst.

scholarly journals Nucleolar stress regulation of endometrial receptivity in mouse models and human cell lines

2019 ◽  
Vol 10 (11) ◽  
Author(s):  
Wei Hu ◽  
Yu-Xiang Liang ◽  
Jia-Mei Luo ◽  
Xiao-Wei Gu ◽  
Zi-Cong Chen ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Early Pregnancy ◽  
Embryo Implantation ◽  
Uterine Receptivity ◽  
Positive Effects ◽  
Delayed Implantation ◽  
Nucleolar Stress ◽  
Pregnant Mice ◽  
Successful Establishment ◽  
Luminal Epithelial Cells

Abstract Embryo implantation is essential to the successful establishment of pregnancy. A previous study has demonstrated that actinomycin D (ActD) could initiate the activation of mouse delayed implantation. However, the mechanism underlying this activation remains to be elucidated. A low dose of ActD is an inducer of nucleolar stress. This study was to examine whether nucleolar stress is involved in embryo implantation. We showed that nucleolar stress occurred when delayed implantation was activated by ActD in mice. ActD treatment also stimulated the Lif-STAT3 pathway. During early pregnancy, nucleolar stress was detected in the luminal epithelial cells during the receptive phase. Blastocyst-derived lactate could induce nucleolar stress in cultured luminal epithelial cells. The inhibition of nucleophosmin1 (NPM1), which was a marker of nucleolar stress, compromised uterine receptivity and decreased the implantation rates in pregnant mice. To translate these mouse data into humans, we examined nucleolar stress in human endometrium. Our data demonstrated that ActD-induced nucleolar stress had positive effects on the embryo attachment by upregulating IL32 expression in non-receptive epithelial cells rather than receptive epithelial cells. Our data should be the first to demonstrate that nucleolar stress is present during early pregnancy and is able to induce embryo implantation in both mice and humans.

scholarly journals Highly metastatic claudin-low mammary cancers can originate from luminal epithelial cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Patrick D. Rädler ◽  
Barbara L. Wehde ◽  
Aleata A. Triplett ◽  
Hridaya Shrestha ◽  
Jonathan H. Shepherd ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Epithelial Cells ◽  
Triple Negative ◽  
Molecular Subtype ◽  
Ras Signaling ◽  
Preneoplastic Lesions ◽  
Independent Manner ◽  
Oncogenic Ras ◽  
Luminal Epithelial Cells

AbstractClaudin-low breast cancer represents an aggressive molecular subtype that is comprised of mostly triple-negative mammary tumor cells that possess stem cell-like and mesenchymal features. Little is known about the cellular origin and oncogenic drivers that promote claudin-low breast cancer. In this study, we show that persistent oncogenic RAS signaling causes highly metastatic triple-negative mammary tumors in mice. More importantly, the activation of endogenous mutant KRAS and expression of exogenous KRAS specifically in luminal epithelial cells in a continuous and differentiation stage-independent manner induces preneoplastic lesions that evolve into basal-like and claudin-low mammary cancers. Further investigations demonstrate that the continuous signaling of oncogenic RAS, as well as regulators of EMT, play a crucial role in the cellular plasticity and maintenance of the mesenchymal and stem cell characteristics of claudin-low mammary cancer cells.

scholarly journals The In Vitro Effect of Steroid Hormones, Arachidonic Acid, and Kinases Inhibitors on Aquaporin 1, 2, 5, and 7 Gene Expression in the Porcine Uterine Luminal Epithelial Cells during the Estrous Cycle

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 832
Author(s):  
Damian Tanski ◽  
Agnieszka Skowronska ◽  
Malgorzata Tanska ◽  
Ewa Lepiarczyk ◽  
Mariusz T. Skowronski
Keyword(s):  
Arachidonic Acid ◽  
Epithelial Cells ◽  
Steroid Hormones ◽  
Estrous Cycle ◽  
Kinase Inhibitor ◽  
Mapk Signaling ◽  
Mapk Kinase ◽  
Vitro Effect ◽  
Luminal Epithelial Cells

Aquaporins (AQPs) are integral membrane proteins, which play an important role in water homeostasis in the uterus. According to the literature, the expression of aquaporins in reproductive structures depends on the local hormonal milieu. The current study investigated the effect of selected PKA kinase inhibitor H89 and MAPK kinase inhibitor PD98059, on the expression of AQP1, 2, 5, and 7, and steroid hormones (E2), progesterone (P4), and arachidonic acid (AA) in the porcine endometrium on days 18–20 and 2–4 of the estrous cycle (the follicular phase where estrogen and follicle-stimulating hormone (FSH) are secreted increasingly in preparation for estrus and the luteal phase where the ovarian follicles begin the process of luteinization with the formation of the corpus luteum and progesterone secretion, respectively). The luminal epithelial cells were incubated in vitro in the presence of the aforementioned factors. The expression of mRNA was determined by the quantitative real-time PCR technique. In general, in Experiment 1, steroid hormones significantly increased expression of AQP1, 2, and 5 while arachidonic acid increased expression of AQP2 and AQP7. On the other hand, MAPK kinase inhibitor significantly decreased the expression of AQP1 and 5. In Experiment 2, E2, P4, or AA combined with kinase inhibitors differentially affected on AQPs expression. E2 in combination with PKA inhibitor significantly decreased expression of AQP1 but E2 or P4 combined with this inhibitor increased the expression of AQP5 and 7. On the contrary, E2 with PD98059 significantly increased AQP5 and AQP7 expression. Progesterone in combination with MAPK kinase inhibitor significantly downregulated the expression of AQP5 and upregulated AQP7. Arachidonic acid mixed with H89 or PD98059 caused a decrease in the expression of AQP5 and an increase of AQP7. The obtained results indicate that estradiol, progesterone, and arachidonic acid through PKA and MAPK signaling pathways regulate the expression of AQP1 and AQP5 in the porcine luminal epithelial cells in the periovulatory period.

Involvement of Nestin in the Progression of Canine Mammary Carcinoma

2021 ◽  
pp. 030098582110186
Author(s):  
Hisashi Yoshimura ◽  
Maiko Moriya ◽  
Ayaka Yoshida ◽  
Masami Yamamoto ◽  
Yukino Machida ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mammary Carcinoma ◽  
Mammary Tumors ◽  
Carcinoma Cells ◽  
Nestin Expression ◽  
Mammary Carcinomas ◽  
Canine Mammary Carcinoma ◽  
Canine Mammary Tumors ◽  
Mammary Carcinoma Cells ◽  
Luminal Epithelial Cells

Nestin, a class VI intermediate filament protein, is known to be expressed in various types of human neoplasms, including breast cancer, and is associated with their progression. However, its expression and role in canine mammary tumors remain unknown. We analyzed nestin expression in canine mammary tumors using in situ hybridization and immunohistochemistry. We also investigated its role in a canine mammary carcinoma cell line using RNA interference. Nestin expression was not observed in luminal epithelial cells of any of the 62 cases of benign mammary lesions examined, although myoepithelial cells showed its expression in most cases. In 16/50 (32%) primary mammary carcinomas and 6/15 (40%) metastases of mammary carcinomas, cytoplasmic nestin expression was detected in luminal epithelial cells. In luminal cells of primary mammary carcinomas, its expression was positively related to several pathological parameters that indicate high-grade malignancy, including histological grading ( P < .01), vascular/lymphatic invasion ( P < .01), Ki-67 index ( P < .01), and metastasis ( P < .05). Immunohistochemistry revealed that nestin expression was related to vimentin expression in mammary carcinomas ( P < .01). This relationship was confirmed using reverse transcription-quantitative polymerase chain reaction using 9 cell lines derived from canine mammary carcinoma ( P < .01). Finally, nestin knockdown in canine mammary carcinoma cells using small interfering RNA inhibited cell proliferation and migration based on WST-8, Boyden chamber, and cell-tracking assays. These findings suggest that nestin may at least partially mediate these behaviors of canine mammary carcinoma cells.

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