Talin1 regulates the endometrial epithelial cell adhesive capacity by interacting with LASP1 and Vitronectin

Abstract

The endometrium is a highly complex tissue that is vulnerable to subtle gene expression changes and is the first point of contact for an implanting blastocyst. Talin1 has previously been identified to regulate cytoskeleton and cell motility, however it has not been investigated in association with infertility. Herein, we presented that Talin1 dysregulation in the missed abortion endometrium would negatively influence endometrial adhesive capacity. Mechanistically, intracellular Talin1 inhibited the nuclear transportation of LIM and SH3 protein 1 (LASP1) and restored the expression of adhesion-associated protein. Moreover, extracellular Talin1 enforces endometrial epithelial cell adhesive capacity by interacting with Vitronectin (VTN) and activating the FAK/Src/ERK signalling pathway. This finding provides a novel insight into the potential use of Talin1 for managing endometrial epithelia cell adhesion. This study represents the first demonstration of Talin1 function in endometrial epithelial cell adhesion and endometrial receptivity. Our findings indicate that re-expression of Talin1 might represent a useful strategy for preventing and treating early pregnancy failure and infertility.

Keywords: Endometrial receptivity; LASP1; Talin1; Vitronectin.