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Differential transferrin expression in placentae from normal and abnormal pregnancies: a pilot study

Alena Kralova1 email, Marta Svetlikova2 email, Jindrich Madar3 email, Zdena Ulcova-Gallova4 email, Antonin Bukovsky2 email and Jana Peknicova1 email

1Institute of Biotechnology, Academy of Sciences of the Czech Republic, v.v.i., 142 20, Prague, Czech Republic

2The University of Tennessee Graduate School of Medicine, Knoxville, TN 37920, USA

3Institute for the Care of Mother and Child, 147 10, Prague, Czech Republic

4Department of Gynaecology and Obstetrics, 304 60, Pilsen, Czech Republic

author email corresponding author email

Reproductive Biology and Endocrinology 2008, 6:27doi:10.1186/1477-7827-6-27

Published: 2 July 2008

Abstract

Background

The placenta is an important site for iron metabolism in humans. It transfers iron from the mother to the fetus. One of the major iron transport proteins is transferrin, which is a blood plasma protein crucial for iron uptake. Its localization and expression may be one of the markers to distinguish placental dysfunction.

Methods

In the experimental study we used antibody preparation, mass spectrometric analysis, biochemical and immunocytochemical methods for characterization of transferrin expression on the human choriocarcinoma cell line JAR (JAR cells), placental lysates, and cryostat sections. Newly designed monoclonal antibody TRO-tf-01 to human transferrin was applied on human placentae from normal (n = 3) and abnormal (n = 9) pregnancies.

Results

Variations of transferrin expression were detected in villous syncytiotrophoblast, which is in direct contact with maternal blood. In placentae from normal pregnancies, the expression of transferrin in the syncytium was significantly lower (p < 0.001) when compared to placentae from abnormal ones (gestational diabetes, pregnancy induced hypertension, drug abuse).

Conclusion

These observations suggest that in the case of abnormal pregnancies, the fetus may require higher levels of transferrin in order to prevent iron depletion due to the stress from the placental dysfunction.


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