Document Detail


Decidual natural killer cell interactions with trophoblasts are impaired in pregnancies at increased risk of preeclampsia.
MedLine Citation:
PMID:  24103555     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Transformation of the uterine spiral arteries (SAs) during pregnancy is critical to support the developing fetus, and is impaired in some pregnancy disorders, including preeclampsia. Decidual natural killer (dNK) cells play a role in SA remodeling, although their interactions with fetal trophoblast remain unclear. A uterine artery Doppler resistance index (RI) in the first trimester of pregnancy can be used as a proxy measure of the extent of SA remodeling; we have used this technique to characterize dNK cells from pregnancies with normal (normal RI) and impaired (high RI) SA remodeling, which display least and highest risk of developing preeclampsia, respectively. We examined the impact of dNK cell secreted factors on trophoblast motility, chemoattraction, and signaling pathways to determine the contribution of dNK cells to SA transformation. We demonstrated that the chemoattraction of the trophoblast by dNK cells is impaired in pregnancies with high RI, as is the ability to induce trophoblast outgrowth from placental villous explants. These processes are dependent on activation of the extracellular signal-regulated kinase 1/2 and phosphatidylinositol 3-kinase-Akt signaling pathways, which were altered in trophoblasts incubated with secreted factors from dNK cells from high RI pregnancies. Therefore, by characterizing pregnancies using uterine artery Doppler RI before dNK cell isolation, we have identified that impaired dNK-trophoblast interactions may lead to poor placentation. These findings have implications for pregnancy pathological conditions, such as preeclampsia.
Authors:
Alison E Wallace; Amanda J Host; Guy S Whitley; Judith E Cartwright
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Publication Detail:
Type:  Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't     Date:  2013-10-06
Journal Detail:
Title:  The American journal of pathology     Volume:  183     ISSN:  1525-2191     ISO Abbreviation:  Am. J. Pathol.     Publication Date:  2013 Dec 
Date Detail:
Created Date:  2013-11-25     Completed Date:  2014-07-02     Revised Date:  2014-10-16    
Medline Journal Info:
Nlm Unique ID:  0370502     Medline TA:  Am J Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1853-61     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2013 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Adult
Chemotaxis / immunology
Decidua* / immunology,  pathology
Female
Humans
Killer Cells, Natural* / immunology,  pathology
MAP Kinase Signaling System / immunology
Mitogen-Activated Protein Kinase 1 / immunology
Mitogen-Activated Protein Kinase 3 / immunology
Phosphatidylinositol 3-Kinases / immunology
Pre-Eclampsia* / immunology,  pathology
Pregnancy
Pregnancy Proteins / immunology
Proto-Oncogene Proteins c-akt / immunology
Risk Factors
Trophoblasts* / immunology,  pathology
Grant Support
ID/Acronym/Agency:
091550//Wellcome Trust
Chemical
Reg. No./Substance:
0/Pregnancy Proteins; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.24/MAPK1 protein, human; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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