scholarly journals A gene network of uterine luminal epithelium organizes mouse blastocyst implantation

2022 ◽  
Vol 21 (1) ◽  
Author(s):  
Shizu Aikawa ◽  
Yasushi Hirota ◽  
Yamato Fukui ◽  
Chihiro Ishizawa ◽  
Rei IIda ◽  
...  
Keyword(s):  
Gene Network ◽  
Luminal Epithelium ◽  
Mouse Blastocyst ◽  
Blastocyst Implantation

Progestin increases cathepsin D synthesis in uterine luminal epithelial cells

1983 ◽  
Vol 244 (5) ◽  
pp. E442-E446 ◽  
Author(s):  
B. C. Moulton ◽  
B. B. Koenig
Keyword(s):  
Epithelial Cells ◽  
Cathepsin D ◽  
Hormonal Control ◽  
Ovariectomized Rats ◽  
Luminal Epithelium ◽  
Progesterone Secretion ◽  
Blastocyst Implantation ◽  
Lysosomal Proteinase ◽  
Cathepsin D Activity ◽  
Luminal Epithelial Cells

Early in blastocyst implantation, cells of the uterine luminal epithelium deteriorate and die in response to the presence of the blastocyst. Destruction of the epithelial cells appears to depend on control of the autophagic activity and enzyme content of lysosomes in these cells. Concentrations of the lysosomal proteinase, cathepsin D, have been identified in luminal epithelial cells, and these studies examined changes in epithelial cathepsin D activity and their hormonal control during early pseudopregnancy in the rat. Cathepsin D activity in luminal epithelial cells increases during early pseudopregnancy to maximal levels at the time of sensitivity to deciduogenic stimuli. Rates of cathepsin D synthesis in luminal epithelial cells also increase during early pseudopregnancy, but neither enzyme activity nor rates of synthesis increase in stromal-myometrial tissues. In ovariectomized rats, progestins rather than estradiol increase cathepsin D activity and rates of synthesis in luminal epithelial cells. These studies suggest that cell death in the luminal epithelium during blastocyst implantation may depend in part on the accumulation of lysosomal cathepsin D in these cells in response to progesterone secretion during early pregnancy.

Paracrine effects of bFGF and KGF on the process of mouse blastocyst implantation

1998 ◽  
Vol 50 (1) ◽  
pp. 54-62 ◽  
Author(s):  
Fuminori Taniguchi ◽  
Tasuku Harada ◽  
Souichi Yoshida ◽  
Tomio Iwabe ◽  
Yoshimasa Onohara ◽  
...  
Keyword(s):  
Mouse Blastocyst ◽  
Paracrine Effects ◽  
Blastocyst Implantation

Involvement of protease in mouse blastocyst implantation in vitro

1980 ◽  
Vol 13 (1) ◽  
pp. 99
Author(s):  
Harumi Kubo ◽  
Akiko I. Spindle
Keyword(s):  
Mouse Blastocyst ◽  
Blastocyst Implantation

scholarly journals Evidence for cross-talk between the LH receptor and LH during implantation in mice

2013 ◽  
Vol 25 (3) ◽  
pp. 511 ◽  
Author(s):  
Virginie Gridelet ◽  
Marie Tsampalas ◽  
Sarah Berndt ◽  
Marie-Thérèse Hagelstein ◽  
Chantal Charlet-Renard ◽  
...  
Keyword(s):  
Mouse Model ◽  
Luteinising Hormone ◽  
Rt Pcr ◽  
Mouse Blastocyst ◽  
Chain Reaction ◽  
Lh Receptor ◽  
Blastocyst Implantation ◽  
Polymerase Chain ◽  
Endometrial Epithelium ◽  
Model Expression

The present study investigated the first interaction that occurs between the blastocyst and endometrium during implantation. Given the ethical objections to studying implantation in humans, a mouse model was used to study the dialogue between luteinising hormone (LH) and luteinising hormone receptor (LHCGR). Several studies performed on LHCGR-knockout mice have generated controversy regarding the importance of the dialogue between LH and LHCGR during implantation. There has been no demonstration of a bioactive LH-like signal produced by the murine blastocyst. The first aim of the present study was to examine and quantify, using radioimmunoassay, the generation of a bioactive LH signal by the murine blastocyst. We went on to examine and quantify endometrial Lhcgr expression to validate the mouse model. Expression of LHCGR in mouse uteri was demonstrated using immunohistochemistry and western blot analysis. To quantify the expression of Lh in the mouse blastocyst and Lhcgr in the endometrium, reverse transcription–polymerase chain reaction (RT-PCR) and real-time quantitative (q) RT-PCR were performed. The results demonstrate that Lhcgr expression in BALB/c mouse endometrial epithelium is increased at the time of implantation and indicate that LHCGR may contribute to the implantation process. In support of this hypothesis, we identified a bioactive LH signal at the time of murine blastocyst implantation.

Dual source and target of heparin-binding EGF-like growth factor during the onset of implantation in the hamster

Development ◽  
2002 ◽  
Vol 129 (17) ◽  
pp. 4125-4134
Author(s):  
Xiaohong Wang ◽  
Haibin Wang ◽  
Hiromichi Matsumoto ◽  
Shyamal K. Roy ◽  
Sanjoy K. Das ◽  
...  
Keyword(s):  
Growth Factor ◽  
Nuclear Receptor ◽  
Similar Pattern ◽  
Implantation Site ◽  
Luminal Epithelium ◽  
Molecular Signaling ◽  
Heparin Binding ◽  
Important Mediator ◽  
Dual Source ◽  
Blastocyst Implantation

Heparin binding EGF-like growth factor (HB-EGF), encoded by the Hegfl gene, is considered as an important mediator of embryo-uterine interactions during implantation in mice. However, it is unknown whether HB-EGF is important for implantation in species with different steroid hormonal requirements. In mice and rats, maternal ovarian estrogen and progesterone (P4) are essential to implantation. In contrast, blastocyst implantation can occur in hamsters in the presence of P4 alone. To ascertain whether HB-EGF plays any role in implantation in hamsters, we examined the expression, regulation and signaling of HB-EGF in the hamster embryo and uterus during the periimplantation period. We demonstrate that both the blastocyst and uterus express HB-EGF during implantation. Hegfl is expressed solely in the uterine luminal epithelium surrounding the blastocyst prior to and during the initiation of implantation. Hypophysectomized P4-treated pregnant hamsters also showed a similar pattern of implantation-specific Hegfl expression. These results suggest that uterine Hegfl expression at the implantation site is driven by either signals emanating from the blastocyst or maternal P4, but not by maternal estrogen. However, in ovariectomized hamsters, uterine induction of Hegfl requires the presence of estrogen and activation of its nuclear receptor (ER), but not P4. This observation suggests an intriguing possibility that an estrogenic or unidentified signal from the blastocyst is the trigger for uterine HB-EGF expression. An auto-induction of Hegfl in the uterus by blastocyst-derived HB-EGF is also a possibility. We further observed that HB-EGF induces autophosphorylation of ErbB1 and ErbB4 in the uterus and blastocyst. Taken together, we propose that HB-EGF production and signaling by the blastocyst and uterus orchestrate the ‘two-way’ molecular signaling to initiate the process of implantation in hamsters.

scholarly journals The potential role of stem cell factor and its receptor c-kit in the mouse blastocyst implantation

1999 ◽  
Vol 5 (9) ◽  
pp. 874-879 ◽  
Author(s):  
Masahiro Mitsunari ◽  
Tasuku Harada ◽  
Masahiro Tanikawa ◽  
Tomio Iwabe ◽  
Fuminori Taniguchi ◽  
...  
Keyword(s):  
Stem Cell ◽  
Stem Cell Factor ◽  
Potential Role ◽  
Mouse Blastocyst ◽  
Blastocyst Implantation

scholarly journals Mining the Mouse Transcriptome of Receptive Endometrium Reveals Distinct Molecular Signatures for the Luminal and Glandular Epithelium

Endocrinology ◽  
2006 ◽  
Vol 147 (7) ◽  
pp. 3375-3390 ◽  
Author(s):  
Andrea L. Niklaus ◽  
Jeffrey W. Pollard
Keyword(s):  
Metal Ion ◽  
Molecular Signature ◽  
Luminal Epithelium ◽  
Innate Immune Responses ◽  
Metal Ion Binding ◽  
Mouse Uterus ◽  
Epithelial Compartment ◽  
Blastocyst Implantation ◽  
Sense And Respond ◽  
Mouse Transcriptome

Epithelia coat most tissues where they sense and respond to the environment and participate in innate immune responses. In the adult mouse uterus, columnar epithelium lines the central lumen and the glands that penetrate the underlying stroma. A nidatory surge of estrogen causes differentiation of the luminal epithelium to the receptive state that permits blastocyst attachment and allows subsequent implantation. Here, using laser-capture microdissection to isolate the luminal and glandular epithelia separately, we have profiled gene expression 2 h before embryo attachment to determine whether there are unique roles for these two epithelial structures in this process. Although most genes were expressed in both compartments, there was greater expression of 153 and 118 genes in the lumen and glands, respectively. In the luminal epithelium, there is enrichment in lipid, metal-ion binding, and carbohydrate-metabolizing enzymes, whereas in the glands, immune response genes are emphasized. In situ hybridization to uterine sections obtained from mice during the preimplantation period validated these data and indicated an array of previously undocumented genes expressed with unique patterns in these epithelia. The data show that each epithelial compartment has a distinct molecular signature and that they act differentially and synergistically to permit blastocyst implantation.

Regulation of sialomucin complex/Muc4 in the female rat reproductive tract

2001 ◽  
Vol 29 (2) ◽  
pp. 162-166 ◽  
Author(s):  
K. L. Carraway ◽  
N. Idris
Keyword(s):  
Epithelial Cells ◽  
Stromal Cells ◽  
Reproductive Tract ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Luminal Epithelium ◽  
Female Rat ◽  
Glycoprotein Complex ◽  
Blastocyst Implantation ◽  
Sialomucin Complex

Sialomucin complex (SMC/rat Muc4) is a hetero-dimeric glycoprotein complex composed of an anti-adhesive mucin subunit ascites sialoglyco-protein (ASGP)-1 and a transmembrane subunit ASGP-2. SMC expression is tightly regulated in the uterus, and its expression appears to block blastocyst implantation. Expression is controlled by steroid hormone levels in the uterine luminal epithelium, but not the uterine glandular epithelium, oviduct, cervix or vagina. Increased progesterone levels lead to downregulation of SMC in the uterine luminal epithelium at the time of receptivity for implantation. Transforming growth factor β (TGF-β) has been implicated as a factor in uterine progesterone responses. Studies on primary rat uterine luminal epithelial cells showed that both SMC protein and transcript are downregulated by TGF-β1, although SMC expression is not altered by treatments with oestrogen or progesterone. SMC is also down-regulated when epithelial cells are co-cultured with isolated uterine stromal cells. Oestradiol and anti-TGF-β block the stromal cell effect. These data indicate that uterine epithelial cells respond to hormones to downregulate SMC via an indirect effect on stromal cells involving paracrine action of TGF-β.

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