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Placental trophoblast cell differentiation: physiological regulation and pathological relevance to preeclampsia.
MedLine Citation:
PMID:  23276825     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
The placenta is a transient organ that forms during pregnancy to support the growth and development of the fetus. During human placental development, trophoblast cells differentiate through two major pathways. In the villous pathway, cytotrophoblast cells fuse to form multinucleated syncytiotrophoblast. In the extravillous pathway, cytotrophoblast cells acquire an invasive phenotype and differentiate into either 1) interstitial extravillous trophoblasts, which invade the decidua and a portion of the myometrium, or 2) endovascular extravillous trophoblasts, which remodel the maternal vasculature. These differentiation events are tightly controlled by the interplay of oxygen tension, transcription factors, hormones, growth factors, and other signaling molecules. More recently, microRNAs have been implicated in this regulatory process. Abnormal placental development, particularly the limited invasion of trophoblast cells into the uterus and the subsequent failure of the remodeling of maternal spiral arteries, is believed to cause preeclampsia, a severe pregnancy related disorder characterized by hypertension and proteinuria. Oxidative stress, the abnormal production and/or function of signaling molecules, as well as aberrant microRNAs expression have been suggested to participate in the pathogenesis of preeclampsia. Several potential biomarkers for preeclampsia have been identified, creating new opportunities for the development of strategies to diagnose, prevent, and treat this disorder.
Authors:
Lei Ji; Jelena Brkić; Ming Liu; Guodong Fu; Chun Peng; Yan-Ling Wang
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-12-28
Journal Detail:
Title:  Molecular aspects of medicine     Volume:  -     ISSN:  1872-9452     ISO Abbreviation:  Mol. Aspects Med.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2013-1-1     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7603128     Medline TA:  Mol Aspects Med     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012. Published by Elsevier Ltd.
Affiliation:
State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.
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