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Journal of Tropical Medicine
Volume 2012 (2012), Article ID 969243, 8 pages
http://dx.doi.org/10.1155/2012/969243
Research Article

In Vitro Infection of Trypanosoma cruzi Causes Decrease in Glucose Transporter Protein-1 (GLUT1) Expression in Explants of Human Placental Villi Cultured under Normal and High Glucose Concentrations

1Cátedra de Biología Celular, Histología y Embriología, Instituto de Biología Celular, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Ciudad Universitaria, 5016 Córdoba, Argentina
2Cátedra de Histología, Embriología y Genética, IICSHUM, Universidad Nacional de La Rioja, 5300 La Rioja, Argentina
3Division of Environmental Health and Occupational Medicine, National Health Research Institutes, 35053 Zhunan Town, Miaoli County, Taiwan

Received 2 June 2011; Accepted 15 July 2011

Academic Editor: Ulrike Kemmerling

Copyright © 2012 Luciana Mezzano et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Trypanosoma cruzi, the etiologic Chagas' disease agent, induces changes in protein pattern of the human placenta syncytiotrophoblast. The glucose transporter protein-1 (GLUT1) is the primary isoform involved in transplacental glucose transport. We carried out in vitro assays to determine if T. cruzi infection would induce changes in placental GLUT1 protein expression under normal and high concentration of glucose. Using Western blot and immunohistological techniques, GLUT1 expression was determined in normal placental villi cultured under normal or high concentrations of glucose, with or without in vitro T. cruzi infection, for 24 and 48 hours. High glucose media or T. cruzi infection alone reduced GLUT1 expression. A yet more accentuated reduction was observed when infection and high glucose condition took place together. We inform, for the first time, that T. cruzi infection may induce reduction of GLUT1 expression under normal and high glucose concentrations, and this effect is synergic to high glucose concentrations.