Document Detail


The tumour suppressor gene maspin is differentially regulated in cytotrophoblasts during human placental development.
MedLine Citation:
PMID:  11969337     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Identification of factors that play a role in regulating the highly invasive ability of human placental cells throughout gestation will contribute to a better understanding of this unique developmental process. The aims of this study were to determine whether the tumour suppressor gene maspin is present in the human placenta and plays a putative role in the regulation of cytotrophoblast invasion during placental development. The data showed that the expression of maspin mRNA was maximum in term placentae compared to the first and second trimester tissues, and absent in the HTR-SVneo (immortalized extravillous cytotrophoblast), JEG-3 and JAR (choriocarcinoma) cell lines. Maspin protein, detected by Western blot analysis, was twofold higher in the second trimester and 4.4-fold higher in the third trimester compared to the first trimester. Maspin immunohistochemical staining was localized in cytotrophoblasts with increased and more diffuse staining in the second and third trimesters. Corresponding to the period of maximum maspin expression, cytotrophoblasts isolated from term placentae had significantly lower invasive ability as compared to first and second trimester cytotrophoblasts (P< 0.03). Further, addition of recombinant maspin significantly decreased cytotrophoblast invasion in vitro by 40-50 per cent in all three trimesters of gestation. This study provides the first evidence of the temporal expression of maspin during human gestation and suggests a putative role for maspin in regulating the invasive activity of cytotrophoblasts at term. The down-regulation of maspin expression may be critical at the time of implantation and early placental development, whereas upregulation of maspin may serve as a signal for the end of cytotrophoblast invasion and gestation.
Authors:
A Dokras; L M G Gardner; D A Kirschmann; E A Seftor; M J C Hendrix
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Placenta     Volume:  23     ISSN:  0143-4004     ISO Abbreviation:  Placenta     Publication Date:  2002 Apr 
Date Detail:
Created Date:  2002-04-23     Completed Date:  2002-11-12     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8006349     Medline TA:  Placenta     Country:  England    
Other Details:
Languages:  eng     Pagination:  274-80     Citation Subset:  IM    
Copyright Information:
Copyright 2002 Elsevier Science Ltd.
Affiliation:
Department of Obstetrics and Gynecology and Holden Comprehensive Cancer Center, University of Iowa, Iowa City, IA 52242, USA. anuja-dokras@uiowa.edu
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MeSH Terms
Descriptor/Qualifier:
Cell Line
Female
Gene Expression Regulation, Developmental
Genes, Tumor Suppressor*
Humans
Immunohistochemistry
Placenta / growth & development*,  metabolism*
Pregnancy
Pregnancy Trimester, Third
Proteins / genetics*,  metabolism*,  pharmacology
RNA, Messenger / genetics,  metabolism
Recombinant Proteins / pharmacology
Serpins / genetics*,  metabolism*,  pharmacology
Signal Transduction
Trophoblasts / drug effects,  metabolism*
Grant Support
ID/Acronym/Agency:
5K12HD00849/HD/NICHD NIH HHS; CA 75681/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Proteins; 0/RNA, Messenger; 0/Recombinant Proteins; 0/SERPIN-B5; 0/Serpins

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


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