Loss of PRICKLE1 leads to abnormal endometrial epithelial architecture, decreased embryo implantation, and reduced fertility in mice.

ABSTRACT: Successful embryo implantation requires coordinated changes in the uterine luminal epithelium, including structural adaptations, apical-basal polarity shifts, intrauterine fluid resorption, and cellular communication. Planar cell polarity proteins, essential for cell organization, are understudied in the context of uterine physiology and implantation. PRICKLE proteins, components of PCP, are suggested to play critical roles in epithelial polarization and tissue morphogenesis. However, their function in the polarized unicellular layer of endometrial epithelium, which supports embryo implantation, is unknown. We developed an endometrial epithelial-specific knockout of mouse Prickle1 using Lactoferrin-iCre to investigate its role in uterine physiology. Prickle1 ablation i

SUBMITTER: Roberts ER 

PROVIDER: S-EPMC11801272 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature