Research Article
Absence of CD9 reduces endometrial VEGF secretion and impairs uterine repair after parturition
Natsuko Kawano, Kenji Miyado, Noriko Yoshii, Seiya Kanai, Hidekazu Saito, Mami Miyado, Noboru Inagaki, Yasushi Odawara, Toshio Hamatani, Akihiro Umezawa
Published:
April 16, 2014
DOI:
10.1038/srep04701
License:
Copyright © 2014, Macmillan Publishers Limited. All rights reserved2014Macmillan Publishers Limited. All rights reservedThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. The images in this article are included in the article's Creative Commons license, unless indicated otherwise in the image credit; if the image is not included under the Creative Commons license, users will need to obtain permission from the license holder in order to reproduce the image. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/
Abstract
In mammals, uterine epithelium is remodeled cyclically throughout adult life for pregnancy. Despite the expression of CD9 in the uterine epithelium, its role in maternal reproduction is unclear. Here, we addressed this issue by examining uterine secretions collected from patients undergoing fertility treatment and fertilization-competent Cd9−/− mice expressing CD9-GFP in their eggs (Cd9−/−TG). CD9 in uterine secretions was observed as extracellular matrix-like feature, and its amount of the secretions associated with repeated pregnancy failures. We also found that the litter size of Cd9−/−TG female mice was significantly reduced after their first birth. Severely delayed re-epithelialization of the endometrium was then occurred. Concomitantly, vascular endothelial growth factor (VEGF) was remarkably reduced in the uterine secretions of Cd9−/−TG female mice. These results provide the first evidence that CD9-mediated VEGF secretion plays a role in re-epithelialization of the uterus.