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Philippe Boeuf, Aimee Tan, Cleofe Romagosa, Jane Radford, Victor Mwapasa, Malcolm E. Molyneux, Steven R. Meshnick, Nicholas H. Hunt, Stephen J. Rogerson, Placental Hypoxia during Placental Malaria, The Journal of Infectious Diseases, Volume 197, Issue 5, 1 March 2008, Pages 757–765, https://doi.org/10.1086/526521
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Abstract
Background. Placental malaria causes fetal growth retardation (FGR), which has been linked epidemiologically to placental monocyte infiltrates. We investigated whether parasite or monocyte infiltrates were associated with placental hypoxia, as a potential mechanism underlying malarial FGR.
Methods. Westudied the hypoxia markers hypoxia inducible factor (HIF)-1α, vascular endothelial growth factor (VEGF), placental growth factor, VEGF receptor 1 and its soluble form, and VEGF receptor 2. We used real-time polymerase chain reaction (in 59 women) to examine gene transcription, immunohistochemistry (in 30 women) to describe protein expression, and laser-capture microdissection (in 23 women) to examine syncytiotrophoblast-specific changes in gene expression. We compared gene and protein expression in relation to malaria infection, monocyte infiltrates, and birth weight.
Results. We could not associate any hallmark of placental malaria with a transcription, expression, or tissue-distribution profile characteristic of a response to hypoxia, but we found higher HIF-1α levels (P = .0005) and lower VEGF levels (P = .0026) in the syncytiotrophoblasts of cases of malaria than in those of asymptomatic control placentas.
Conclusions. Our data are inconsistent with a role for placental hypoxia in the pathogenesis of malaria-associated FGR. The laser-capture microdissection study was small, but its results suggest (1) that malaria affects syncytiotrophoblast-gene transcription and (2) novel potential mechanisms for placental malaria-associated FGR.
