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Novel insights into molecular mechanisms of abruption-induced preterm birth

Published online by Cambridge University Press:  01 November 2010

Catalin S. Buhimschi*
Affiliation:
Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA.
Frederik Schatz
Affiliation:
Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA.
Graciela Krikun
Affiliation:
Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA.
Irina A. Buhimschi
Affiliation:
Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA.
Charles J. Lockwood
Affiliation:
Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA.
*
*Corresponding author: Catalin S. Buhimschi, Yale University School of Medicine, Department of Obstetrics, Gynecology & Reproductive Sciences, 333 Cedar Street, LLCI 804, New Haven, CT 06520, USA. E-mail: catalin.buhimschi@yale.edu

Abstract

Preterm birth (PTB) complicates more than 12% of all deliveries. Despite significant research, the aetiology of most cases of PTB remains elusive. Two major antecedents of PTB, intra-amniotic infection and decidual haemorrhage (abruption), can exhibit dissimilar demographic and genetic predispositions, despite sharing common molecular and cellular pathways. The use of high-throughput, high-dimensional technologies reveals substantial crosstalk between the coagulation and inflammation pathways. Tissue factor, thrombin and cytokines are key mediators of this crosstalk. Abruptions are associated with excess thrombin generated from decidual-cell-expressed tissue factor. Although thrombin is a primary mediator of the coagulation cascade, it can also promote inflammation-associated PTB by enhancing expression of matrix metalloproteinase and neutrophil-chemoattracting and -activating chemokines. Here, we provide novel insights into the molecular mechanisms and pathways leading to PTB in the setting of placental abruption.

Type
Review Article
Copyright
Copyright © Cambridge University Press 2010

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References

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Further reading, resources and contacts

The International HapMap Project is a partnership of scientists and funding agencies from Canada, China, Japan, Nigeria, the United Kingdom and the U.S.A. to develop a public resource that will help researchers find genes associated with human disease and response to pharmaceuticals. For more information, consulthttp://hapmap.ncbi.nlm.nih.gov/abouthapmap.htmlGoogle Scholar
Online Mendelian Inheritance in Man is a comprehensive compendium of human genes and genetic phenotypes. Information regarding the F5 gene, which encodes coagulation factor V and the 20210G-A mutation in the prothrombin F2 gene, can be found athttp://www.ncbi.nlm.nih.gov/omimGoogle Scholar