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Absence of CD9 reduces endometrial VEGF secretion and impairs uterine repair after parturition.

Authors
  • Kawano, Natsuko
  • Miyado, Kenji
  • Yoshii, Noriko
  • Kanai, Seiya
  • Saito, Hidekazu
  • Miyado, Mami
  • Inagaki, Noboru
  • Odawara, Yasushi
  • Hamatani, Toshio
  • Umezawa, Akihiro
Type
Published Article
Journal
Scientific Reports
Publisher
Springer Nature
Publication Date
Jan 01, 2014
Volume
4
Pages
4701–4701
Identifiers
DOI: 10.1038/srep04701
PMID: 24736431
Source
Medline
License
Unknown

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.

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