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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/16829

Title: Expression of the sFLT1 Gene in Cord Blood Cells Is Associated to Maternal Arsenic Exposure and Decreased Birth Weight
Authors: Remy, Sylvie
Govarts, Eva
BRUCKERS, Liesbeth
Paulussen, Melissa
Wens, Britt
Den Hond, Elly
Nelen, Vera
Baeyens, Willy
van Larebeke, Nicolas
Loots, Ilse
Sioen, Isabelle
Schoeters, Greet
Issue Date: 2014
Citation: PLOS ONE, 9 (3)
Abstract: There is increasing epidemiologic evidence that arsenic exposure in utero is associated with adverse pregnancy outcomes and may contribute to long-term health effects. These effects may occur at low environmental exposures but the underlying molecular mechanism is not clear. We collected cord blood samples of 183 newborns to identify associations between arsenic levels and birth anthropometric parameters in an area with very low arsenic exposure. Our core research aim was to screen for transcriptional marks that mechanistically explain these associations. Multiple regression analyses showed that birth weight decreased with 47 g (95% CI: 16–78 g) for an interquartile range increase of 0.99 mg/L arsenic. The model was adjusted for child’s sex, maternal smoking during pregnancy, gestational age, and parity. Higher arsenic concentrations and reduced birth weight were positively associated with changes in expression of the sFLT1 (soluble fms-like tyrosine kinase-1) gene in cord blood cells in girls. The protein product of sFLT1 is a scavenger of vascular endothelial growth factor (VEGF) in the extracellular environment and plays a key role in the inhibition of placental angiogenesis. In terms of fetal development, inhibition of placental angiogenesis leads to impaired nutrition and hence to growth retardation. Various genes related to DNA methylation and oxidative stress showed also changed expression in relation to arsenic exposure but were not related to birth outcome parameters. In conclusion, this study suggests that increased expression of sFLT1 is an intermediate marker that points to placental angiogenesis as a pathway linking prenatal arsenic exposure to reduced birth weight.
URI: http://hdl.handle.net/1942/16829
DOI: 10.1371/journal.pone.0092677
ISI #: 000333459900096
ISSN: 1932-6203
Category: A1
Type: Journal Contribution
Validation: ecoom, 2015
Appears in Collections: Research publications

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