Document Detail


The paracrinology of tubal ectopic pregnancy.
MedLine Citation:
PMID:  21827822     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
As part of successful human reproduction, the Fallopian tube must provide a suitable environment for pre-implantation development of the embryo and for efficient transport of the embryo to the uterus for implantation. These functions are coordinated by paracrine interactions between tubal epithelial, smooth muscle and immune cells and the cells of the developing embryo. Alterations in these signals can lead to a tubal microenvironment encouraging of embryo implantation and to dysregulated tubal motility, ultimately resulting in inappropriate and early implantation of the embryo in the Fallopian tube. Here, we highlight novel and emerging concepts in tubal physiology and pathobiology, such as the induction of a receptive phenotype within the Fallopian tube, leading to ectopic implantation. Chlamydia trachomatis infection is a risk factor for tubal ectopic pregnancy. Activation of toll-like receptor 2 (TLR-2) in the Fallopian tube epithelium, by C. trachomatis has recently been demonstrated, leading to the dysregulation of factors involved in implantation and smooth muscle contractility, such as prokineticins (PROK), activin A and interleukin 1 (IL-1). The Fallopian tube has also recently been shown to harbour a unique population of immune cells, compared to the endometrium. In addition, the complement of immune cells in the Fallopian tube has been reported to be altered in Fallopian tube from women with ectopic pregnancy. There are increasing data suggesting that vascularisation of the Fallopian tube, by the embryo during ectopic pregnancy, differs from that initiated in the uterus during normal pregnancy. This too, is likely the result of paracrine signals between the embryo and the tubal microenvironment.
Authors:
Julie L V Shaw; Andrew W Horne
Publication Detail:
Type:  Journal Article; Review     Date:  2011-07-30
Journal Detail:
Title:  Molecular and cellular endocrinology     Volume:  358     ISSN:  1872-8057     ISO Abbreviation:  Mol. Cell. Endocrinol.     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-05-30     Completed Date:  2012-11-06     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  7500844     Medline TA:  Mol Cell Endocrinol     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  216-22     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
Affiliation:
Department of Laboratory Medicine and Pathobiology, University of Toronto, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8.
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MeSH Terms
Descriptor/Qualifier:
Animals
Embryo, Mammalian / metabolism
Female
Humans
Lymphocytes / metabolism
Muscle, Smooth / metabolism
Neovascularization, Pathologic / metabolism,  pathology
Paracrine Communication*
Pregnancy
Pregnancy, Tubal / immunology,  metabolism*,  pathology
Grant Support
ID/Acronym/Agency:
G0802808//Medical Research Council; G0802808(90914)//Medical Research Council
Comments/Corrections

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