Please use this identifier to cite or link to this item:
Type: Artigo
Title: Delta-like ligand (DLL)1 expression in early mouse decidua and its localization to uterine natural killer cells
Author: Degaki, Karina Y.
Chen, Zhilin
Yamada, Aureo T.
Croy, B. Anne
Abstract: Uterine vascular changes, critical for pregnancy success, occur at each implant site during endometrial decidualization. Mesometrial decidualization recruits high numbers of angiogenic, uterine Natural Killer (uNK) cells that trigger midpregnancy spiral arterial remodeling. We postulated that uNK cells contribute to early decidual angiogenesis as endothelial-cell extrinsic sources of Delta-like ligand 1 (DLL1), a molecule that induces endothelial tip cell differentiation and orthogonal vascular growth in other tissues. Virgin uteri expressed Dll1 mesometrially and anti-mesometrially and relative expression increased in both anatomic regions as pregnancy progressed. Analyses of transcripts from gd10.5 uNK cells flow sorted on the basis of expression of Dolichos biflorus agglutinin (DBA) lectin revealed that DBA+ but not DBA- uNK cells expressed Dll1. Immunostaining at gd4.5 found DLL1-expressing cells rare. At gd6.5, DBA+ uNK cells at all stages of maturation expressed DLL1. By gd10.5, DLL1 immunoreactivity was strongly expressed by some but not all DBA+ uNK cells and more weakly by DBA- cells. DLL1+ cells were mesometrially stratified and concentrated within central decidua basalis. Our data suggest that uNK cells have the potential to induce endothelial tip cell differentiation and to promote non-planar vascular growth within early decidua basalis
Subject: Expressão gênica
Country: Estados Unidos
Editor: Public Library of Science
Rights: Aberto
Identifier DOI: 10.1371/journal.pone.0052037
Date Issue: 2012
Appears in Collections:IB - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
000313051500022.pdf3.43 MBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.