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Results for “Embryo Implantation”

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At least 19 recordsLinked to original sources
PubMed2025

LncRNA Profiling and ceRNA Network Construction of Intrauterine Exosomes in Goats During Embryo Implantation.

Exosomes have been shown to play an important role in embryo implantation, but the mechanism is still unclear. This study aimed to investigate the functional roles of lncRNAs in intrauterine exosomes in goat pregnancy. We used RNA-seq to identify the lncRNA profiles of exosomes obtained from goat uterine rinsing fluid at 5, 15, and 18 days of gestation. In addition, we performed weighted gene co-expression network analysis based on differentially expressed mRNAs (DEMs) and lncRNAs (DELs). Functional enrichment analyses of gene modules were conducted using Gene Ontology classification (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. A lncRNA-miRNA-mRNA competing endogenous RNA (ceRNA) regulatory network was constructed based on predictive interaction derived from miRTarBase, miRDB and RNAhybrid databases. Altogether, 831 DELs were identified. GO and KEGG analysis showed that the target genes were enriched in processes associated with embryo implantation, such as signaling receptor activity, binding and immune response. Nine functional co-expression modules were enriched in various biological processes, such as metabolic pathways, protein transport, cell cycle and VEGF signaling pathway. Additionally, 12 lncRNA-mediated ceRNA networks were constructed. Our results demonstrate that exosomal lncRNAs in uterine flushing fluid exhibit dynamic changes across gestational stages and play an important role in regulating the uterine microenvironment during embryo implantation. These findings provide a foundational basis for screening exosome-derived lncRNAs that influence embryo implantation and contribute to elucidating the mechanistic roles of lncRNAs in exosome-mediated processes during early pregnancy.

embryo implantation↗
PubMed2026

Mammalian DNA methyltransferases in DNA methylation and imprinted gene expression in extraembryonic ectoderm of post-implantation embryos.

DNA methylation in mammals is mainly catalyzed by three DNA methyltransferases (DNMTs). Conventionally, DNMT1 is considered the primary DNMT protein for maintenance DNA methylation, whereas DNMT3A and DNMT3B function in de novo DNA methylation. In two previous studies, we demonstrated that DNMT3A and DNMT3B maintain genome-wide DNA methylation in embryonic stem (ES) cells and in the epiblast of post-implantation embryos. Interestingly, DNMT3A and DNMT3B also sustain genome-wide DNA methylation in the extraembryonic ectoderm (EXE) of post-implantation embryos, including repeats, genic and intergenic regions. Although DNMT1 plays a major role in maintaining DNA methylation at the imprinting control regions (ICRs) in the imprinted regions, DNMT3A and DNMT3B are required for preserving DNA methylation at the ICRs of a subset of imprinted regions in EXE, similar to the observations in ES cells and epiblast. Surprisingly, de novo DNA methylation mediated by DNMT3A and DNMT3B leads to increased DNA methylation at a large subset of imprinted regions. These results are consistent with what we previously elucidated in the epiblast of post-implantation embryos. Importantly, loss of DNA methylation at the ICR of an imprinted region, resulting from the absence of DNMT1 or two DNMT3 proteins, causes allelic expression switch of the corresponding imprinted genes in that imprinted region. This study provides further evidence that DNMT3A and DNMT3B exert both maintenance and de novo DNA methylation functions across the genome in post-implantation embryos. It also validates some previous findings for DNA methylation-dependent allelic expression switch of imprinted genes.

DNA methylation↗
PubMed2025

Mouse totipotent blastomere-like cells model embryogenesis from zygotic genome activation to post implantation.

Embryo development begins with zygotic genome activation (ZGA), eventually generating blastocysts for implantation. However, in vitro systems modeling the pre-implantation development are still absent and challenging. Here, we used mouse totipotent blastomere-like cells (TBLCs) to develop spontaneous differentiation and blastoid formation systems, respectively. We found Wnt signaling enabled the rapid expansion of TBLCs and the optimization of their culture medium. We successfully developed a TBLC-spontaneous differentiation system in which mouse TBLCs (mTBLCs) firstly converted into two types of ZGA-like cells (ZLCs) distinguished by Zscan4 expression. Surprisingly, Zscan4-, but not Zscan4+, ZLCs further passed through intermediate 4-cell and then 8-cell/morula stages to produce epiblast, primitive endoderm, and trophectoderm lineages. Significantly, single TBLCs underwent expansion, compaction, and polarization to efficiently generate blastocyst-like structures and even post-implantation egg-cylinder-like structures. Conclusively, we established TBLC-based differentiation and embryo-like structure formation systems to model early embryonic development, offering criteria for evaluating and understanding totipotency.

Animals↗
PubMed1979

Reproductive failure and maternal-fetal relationship in a Peromyscus species cross.

Mating, fertilization, implantation, prenatal mortality, fetal and placental size, and placental ultrastructure were studied in intraspecific and interspecific crosses involving Peromyscus maniculatus and P. polionotus. Failure to mate was a major factor in interspecific crosses and was much more pronounced in crosses between P. polionotus females and P. maniculatus males than in the reciprocal cross. Failure of implantation following mating, however, was more pronounced in crosses between P. maniculatus females and P. polionotus males. Failure of implanted embryos to survive to term was a factor in crosses between P. polionotus females and P. maniculatus males. Comparison of the placental labyrinth of conceptuses from intraspecific and interspecific crosses revealed no differences at the ultrastructural level. The relationship of these observations to the evolution of isolating mechanisms in mammals and to physiological aspects of the developing maternal-fetal relationship are discussed. A model of placental and fetal size inheritance is presented.

Animals↗
PubMed2026

ENTPD3 as a novel regulator of endometrial receptivity: suppressing EMT via the ATP-P2Y2 axis in patients with recurrent implantation failure.

BACKGROUND: Recurrent implantation failure (RIF) remains a major challenge in assisted reproductive technology and is primarily attributed to impaired endometrial receptivity. Despite its clinical significance, the precise mechanisms underlying RIF remain inadequately understood. METHODS: Single-cell RNA sequencing (scRNA-seq) was performed on endometrial samples from patients with RIF and healthy controls during the secretory phase using the 10X Genomics Chromium platform. The expression and localization of ectonucleoside triphosphate diphosphohydrolase 3 (ENTPD3) in the window of implantation (WOI) in the endometrium were examined using real-time quantitative polymerase chain reaction (RT-qPCR), western blotting, and immunohistochemistry (IHC). A mouse model with ENTPD3 overexpression was utilized to assess embryo implantation in vivo, and an in vitro blastocyst adhesion assay was performed to evaluate endometrial receptivity. Additionally, Ishikawa cells were transduced with an ENTPD3 recombinant adenovirus to explore the underlying molecular mechanisms. RESULTS: ENTPD3 expression was significantly upregulated in the endometria of patients with RIF during the WOI, and its apical surface localization in endometrial epithelial cells was confirmed by single-cell data and IHC. Functional studies demonstrated that ENTPD3 overexpression impaired endometrial receptivity by suppressing epithelial-mesenchymal transition (EMT). In vivo, ENTPD3 overexpression markedly reduced endometrial receptivity and inhibited embryo implantation in mice. Consistently, in vitro assays revealed that ENTPD3 overexpression diminished blastocyst adhesion to endometrial epithelial cells. Mechanistically, ENTPD3 hydrolyzes ATP, thereby suppressing EMT via the P2Y2 signaling pathway and ultimately disrupting endometrial receptivity. CONCLUSIONS: Dysregulated ENTPD3 expression contributes to RIF pathogenesis by impairing endometrial receptivity through ATP hydrolysis-mediated suppression of EMT via P2Y2 signaling. These findings highlight ENTPD3 as a potential therapeutic target for improving implantation success in affected patients.

Female↗
PubMed1979

Gap junctional communication in the post-implantation mouse embryo.

We studied the extent of cell-to-cell communication via junctional channels in in vitro-implanted mouse blastocysts by monitoring ionic coupling and the spread of two injected low molecular weight dyes, fluorescein and Lucifer yellow. In the early attached embryos, both trophoblasts and cells of the inner cell mass (ICM) were ionically coupled to one another. Dye injections in either trophoblasts or ICM cells resulted in spread to the entire embryo. As older and more developed embryos were examined, the spread of injected dye was progressively more limited. In the most developed embryos examined, dye injected into a cell in the ICM region resulted in spread throughout the ICM but not into the surrounding trophoblast cells, while dye injected into a trophoblast cell did not spread to any other cell in the embryo. Simultaneous monitoring of ionic coupling and dye injections in embryos of intermediate stages in this transition revealed that the trophoblast and ICM cells were ionically coupled, even across the apparent boundary where no dye was observed to pass. In the latest stage embryos examined in which no injected dye was observed to move out of the ICM, ionic coupling was still observed between the cells of the ICM and the trophoblasts. Furthermore, in the more developed embryos, dye injected into the ICM region frequently was not transferred to all the cells of the ICM, thus suggesting a further compartmentalization of due spread within the ICM. Our observations that ionic coupling is more extensive than the detectable spread of injected dyes may perhaps reflect a reduced number of junctional channels. With fewer channels less dye would pass between cells, so that, together with continuous quenching, the transfer of injected dye would not be detectable. This partial segregation of cell-to-cell communication as indicated by the limited dye spread may parallel specific differentiation processes, in particular that of giant trophoblast, embryonic ectoderm and extraembryonic endoderm differentiation.

Animals↗
PubMed1978

Localization and synthesis of alphafoetoprotein in post-implantation mouse embryos.

The localization and synthesis of alphafoetoprotein (AFP) during mouse embryogenesis were studied by immunoperoxidase and by immunoprecipitation after radioactive labelling, using an antiserum prepared against AFP. AFP is first detectable in embryos on the 7th day of gestation (7th day embryos). In 7th and 8th day embryos AFP is confined to visceral (proximal) endoderm cells around the embryonic region of the egg cylinder. Visceral extra-embryonic and parietal (distal) endoderm cells do not contain AFP. By the 9th day of gestation AFP is also present in the extra-embryonic ectoderm, mesoderm and embryonic ectoderm cells around the three cavities of the embryo. These tissues do not synthesize AFP when cultured in isolation, but can adsorb AFP when it is added to the medium. On the 12th day of gestation AFP synthesis is confined to the endoderm layer of the visceral yolk sac. It is concluded that the ability to synthesize AFP is a property which is restricted to the visceral endoderm during early post-implantation development. The presence of AFP in other tissues of the embryo appears to be due to adsorption.

Animals↗
PubMed1977

[Effect of aminopterin on pre-implantation rat embryos cultivated outside the body].

The rat embryos at the stage of 8 blastomeres were explanted in the Biggers' medium with 20% of blood serum from the rats obtained different doses of aminopterin. The marked delay of cleavage rate, morphological anomalies of blastocysts, selective damaging effect of aminopterin upon the inner cells mass (embryoblast) and high resistance of trophectoderm cells against this drug were observed. The role of dihydrololate reductase at the preimplantation developmental stages, the resistance against aminopterin of the early rat embryos within the maternal organism and high sensitivity to this drug of the embryos in vitro are discussed. A conclusion is drawn on the presence of the barrier function of oviducts with respect to aminopterin.

Aminopterin↗
PubMed2026

Enhancer-promoter interaction maps in pig implantation tissue identify candidate cis-regulatory elements and regulatory variants.

Due to the polygenic nature of pig reproductive traits, most variants accounting for the phenotypic variation remain poorly characterized. It is well established that trait-associated variants are often enriched in regulatory elements of relevant tissues, and coordinated endometrial-conceptus crosstalk is critical for implantation success. Accordingly, this study aimed to investigate the chromatin landscape in pig endometrium-conceptus tissues and identify regulatory variants associated with reproductive traits. Combining RNA-seq and ChIP-seq, we uncovered cis-regulatory elements whose histone modification patterns correlate with gene expression. H3K27ac-based chromatin interaction profiling further resolved 2137 cis-regulatory elements involved in enhancer-promoter (E-P) interactions. Subsequent analyses identified candidate variants within these regulatory regions that associate with reproductive traits, in which the enhancer SNP rs346038249 likely affects transcriptional activity through allele-dependent transcription factor binding. Collectively, our findings provide mechanistic insights into pig embryo implantation and nominate candidate regulatory variants that merit further functional validation for their potential role in pig genetic improvement.

Embryo implantation↗
PubMed2025

Genotyping of natural killer cell immunoglobulin-like receptors in human early reproductive losses.

Genotyping of killer cell immunoglobulin-like receptors (KIR) of NK-cells was performed in 634 women with early pregnancy losses (EPL), including 158 women with recurrent implantation failure (RIF) after at least three IVF cycles, and 110 women with at least two intrauterine pregnancy losses characterized by clinically confirmed retention of a non-viable fetus in the uterus without spontaneous miscarriage, defined as recurrent pregnancy loss (RPL). The control group consisted of 431 women with at least two healthy children. In the RIF, a significant shift in the frequency of KIR-genotypes was observed compared with both the control and the RPL groups. A significantly higher frequency of the KIR-AA genotype was observed in the RIF group compared to the control group (&#x3c7;&#xb2; = 26.78; p&#x202f;<&#x202f;0.0001; OR = 2.7) and the RPL group (&#x3c7;&#xb2; = 15.83; p&#x202f;<&#x202f;0.0001; OR = 2.86). Analysis of the frequency of full-length/deletion alleles of KIR2DS4 among AA genotype carriers showed an increased frequency of the 2DS4-del in the RIF compared with the RPL and control groups. A significantly higher frequency of the cenAA was also observed in RIF compared with the control (&#x3c7;&#xb2; = 20.10; p&#x202f;<&#x202f;0.0001) and the RPL(&#x3c7;&#xb2; = 12.05; p&#x202f;<&#x202f;0.005). The significantly increased frequency of the KIR-AA genotype with predominance of deletion KIR2DS4 alleles, along with the elevated frequency of the cenAA in RIF, may indicate insufficient NK-cell activation at the stage of embryo implantation. These findings suggest different etiological mechanisms for RIF and RPL.

Humans↗
PubMed1976

Alternative explanations of the differing behaviour of ovarian and testicular teratomas.

There are several aspects of the biology of teratomas which may be important in the aetiology of malignant versus non-malignant forms. Firstly, the ages when malignant teratomas form in the ovary (children) and testis (adult) follow by a similar span of years the time of oogenesis (fetus) and spermatogenesis (onset at puberty) and, specifically, follow by less than a decade the periods of active mitosis and meiosis during which interconnection of germ cells by intercellular bridges occurs. Secondly, ovarian teratomas may be viewed as parthenogenically activated oocytes, while testicular teratocarcinomas may represent post-meiotic fusion events more comparable to fertilisation; the malignant potential in the latter case could relate to fundamental differences in male and femal germ plasm. Thirdly,, the fact that malignant teratomas are easily produced by transplanting early embryos to extrauterine sites, while there is loss of malignancy with differentiation within a tumour or when malignant cells are injected into pre-implantation embryos and contribute cells to a variety of normal tissues, suggests that the malignant potential of teratomas has to do with gene control rather than mutational events.

Adolescent↗
PubMed2025

A long noncoding RNA with enhancer-like function in pig zygotic genome activation.

The zygotic genome activation (ZGA) is crucial for the development of pre-implantation embryos. Long noncoding RNAs (lncRNAs) play significant roles in many biological processes, but the study on their role in the early embryonic development of pigs is limited. In this study, we identify lncFKBPL as an enhancer-type lncRNA essential for pig embryo development. lncFKBPL is expressed from the 4-cell stage to the morula stage in pig embryos, and interference with lncFKBPL leads to a developmental arrest at the 8-cell stage. Mechanistic investigations uncover that lncFKBPL is able to bind to MED8, thereby mediating enhancer activity and regulating FKBPL expression. Additionally, FKBPL interacts with the molecular chaperone protein HSP90AA1, stabilizing CDK9 and boosting its protein-level expression. Elevated CDK9 levels enhance Pol II phosphorylation, facilitating ZGA. Our findings illuminate the role of lncFKBPL as an enhancer lncRNA in pig ZGA regulation and early embryo development, providing a foundation for further exploration in this area.

Animals↗