Oral Presentation Society of Obstetric Medicine of Australia and New Zealand and Australasian Diabetes in Pregnancy Society Joint Scientific Meeting 2017

Effect of placental growth factor on trophoblast integration into endothelial cell networks in the presence of inflammation (#62)

Katrina Chau 1 , Bei Xu 1 , Annemarie Hennessy 1 , Angela Makris 2
  1. Vascular Immunology Group , Heart Research Institute, Newtown, NSW, Australia
  2. Renal Unit, Liverpool Hospital, Liverpool, NSW, Australia

Introduction: Invasion of maternal spiral arterioles by trophoblast cells is fundamental to normal placental development. Abnormal spiral arteriole remodelling is often present in pregnancies affected by preeclampsia. Placental growth factor (PlGF) is produced by the placenta and this molecule is decreased during early pregnancy of women with preeclamptic pregnancy as compared to unaffected women. The influence of PlGF on the processes of early placentation is not known.

Objectives: To observe the effect of supplemental PlGF upon capillary-like uterine endothelial cell networks and a first trimester human trophoblast cell line in the presence or absence of inflammation induced by exogenous tumour necrosis factor-alpha.

Methods: 24-well tissue culture plates were coated with 300 uL of undiluted Matrigel and allowed to gelatinise at 37oC for 30 minutes. Fluorescent labelled uterine myometrial microvascular endothelial cells and HTR8/SVNeo cells were co-cultured (1 X 105 per well) for 20 hours treated with PlGF (10 ng/mL) and /or TNF-alpha (0.5 ng/mL). Images were captured by fluorescence microscopy and analysed using ImageJ. Experiments were repeated 8 times, data was analysed using SPSS v24.

Results: TNF alpha reduced trophoblast cell integration into endothelial networks (Control vs TNF p = 0.03) but this was not ameliorated by addition of PlGF (TNF vs TNF + PLGF p = 0.51). Furthermore, PlGF supplementation itself did not improve cell integration (Control vs PlGF p = 0.48).

Conclusions: Placental growth factor does not improve trophoblast cell integration into endothelial cell networks nor reverse the inhibitory effect of TNF alpha.