Endometrial profilin 1: a key player in embryo-endometrial crosstalk
العنوان: | Endometrial profilin 1: a key player in embryo-endometrial crosstalk |
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المؤلفون: | Seon-Hwa Hong, Dong Hee Choi, Chang-Jin Lee, Jung-Jae Ko, Youn-Jung Kang, Min-Ji Yoon, Jee Hyun Kim, Hwang Kwon, Kyung-Ah Lee, Hwa Seon Koo |
المصدر: | Clinical and Experimental Reproductive Medicine |
بيانات النشر: | The Korean Society for Reproductive Medicine, 2020. |
سنة النشر: | 2020 |
مصطلحات موضوعية: | 0301 basic medicine, Regulator, Embryo, Biology, Endometrium, Profilin 1, Cell biology, 03 medical and health sciences, Crosstalk (biology), 030104 developmental biology, 0302 clinical medicine, medicine.anatomical_structure, Reproductive Medicine, Embryo attachment, Profilin-1, 030220 oncology & carcinogenesis, Embryo implantation, medicine, Cell-cell adhesion, Original Article, Cytoskeleton, Cell shape, Actin cytoskeletal network, Actin |
الوصف: | Objective: Despite extensive research on implantation failure, little is known about the molecular mechanisms underlying the crosstalk between the embryo and the maternal endometrium, which is critical for successful pregnancy. Profilin 1 (PFN1), which is expressed both in the embryo and in the endometrial epithelium, acts as a potent regulator of actin polymerization and the cytoskeletal network. In this study, we identified the specific role of endometrial PFN1 during embryo implantation.Methods: Morphological alterations depending on the status of PFN1 expression were assessed in PFN1-depleted or control cells grown on Matrigel-coated cover glass. Day-5 mouse embryos were cocultured with Ishikawa cells. Comparisons of the rates of F-actin formation and embryo attachment were performed by measuring the stability of the attached embryo onto PFN1-depleted or control cells.Results: Depletion of PFN1 in endometrial epithelial cells induced a significant reduction in cell-cell adhesion displaying less formation of colonies and a more circular cell shape. Mouse embryos co-cultured with PFN1-depleted cells failed to form actin cytoskeletal networks, whereas more F-actin formation in the direction of surrounding PFN1-intact endometrial epithelial cells was detected. Furthermore, significantly lower embryo attachment stability was observed in PFN1-depleted cells than in control cells. This may have been due to reduced endometrial receptivity caused by impaired actin cytoskeletal networks associated with PFN1 deficiency.Conclusion: These observations definitively demonstrate an important role of PFN1 in mediating cell-cell adhesion during the initial stage of embryo implantation and suggest a potential therapeutic target or novel biomarker for patients suffering from implantation failure. |
تدمد: | 2233-8241 2233-8233 |
DOI: | 10.5653/cerm.2019.03454 |
URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::143fcf9cfc25a9215b90c5e83b71471b https://doi.org/10.5653/cerm.2019.03454 |
Rights: | OPEN |
رقم الانضمام: | edsair.doi.dedup.....143fcf9cfc25a9215b90c5e83b71471b |
قاعدة البيانات: | OpenAIRE |
تدمد: | 22338241 22338233 |
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DOI: | 10.5653/cerm.2019.03454 |