Abstract
Background: Blastocyst implantation mainly depends on the adhesion between cells and the cell matrix. Endometrial adhesion plays an important role in establishing endometrial receptivity, but its molecular mechanism remains unclear. Talin1 is a local adhesion complex protein necessary for cell adhesion and movement. However, the role and mechanism of Talin1 in embryo implantation remain unclear. Methods: The expression levels of Talin1 and Integrin αvβ3 were measured in the receptive endometrium from the URPL cohort and NC cohort. A JEG-3 trophoblast and endometrial epithelial cell adhesion model and pregnant mouse model were established. The molecular mechanism of Talin1-mediated regulation of cell adhesion was explored by adhesion experiments, RNA sequencing, RT-qPCR and western blotting assays. Findings: Talin1 enhances endometrial cell adhesion and endometrial receptivity by regulating the activity of the Ras signaling pathway, and it ultimately facilitates embryo implantation. Interpretation: This study revealed the specific molecular mechanism of the pathogenesis of UPRL caused by endometrial receptivity insufficiency in cell and animal models. We should conduct additional pharmacological research on the Ras signaling pathway and provide new therapeutic targets for URPL. Funding: This study was supported by grants from the National Natural Science Foundation of China and the Natural Science Foundation of Guangxi Zhuang Autonomous Region and the Guangxi Medical University Training Program for Distinguished Young Scholars Declaration of Interests: The authors declare that they have no conflicts of interest. Ethics Approval Statement: All participants provided written informed consent, and the study was approved by the Ethics Committee of the First Affiliated Hospital of Guangxi Medical University. All animal experimental procedures were approved by the animal ethics committee of Guangxi Medical University in accordance with animal research guidelines.
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