Endometrial profilin 1: A key player in embryo-endometrial crosstalk

• Published in: Clinical and experimental reproductive medicine Vol. 47; no. 2; pp. 114 - 121
• Main Authors: Lee, Chang-Jin, Hong, Seon-Hwa, Yoon, Min-Ji, Lee, Kyung-Ah, Ko, Jung-Jae, Koo, Hwa Seon, Kim, Jee Hyun, Choi, Dong Hee, Kwon, Hwang, Kang, Youn-Jung
• Format: Journal Article
• Language: Korean
• Published: 2020
• Subjects: Actin cytoskeletal network; Embryo implantation; Cell-cell adhesion; Profilin 1; Embryo attachment
• ISSN: 2233-8233; 2233-8241

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.