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Endocrine Abstracts (2014) 36 OC4.3 | DOI: 10.1530/endoabs.36.OC4.3

BSPED2014 Oral Communications Oral Communications 4 (9 abstracts)

A role for delta-like homologue 1 in a secretory placental population and implications for fetal growth

Muriel Meso 1 , Harshini Katugampola 1 , Joe Aquilina 2 , Rebecca Allen 2 , Shemoon Marleen 2 , Helen Storr 1 , Leo Dunkel 1 & Marika Charalambous 1


1William Harvey Research Institute, Centre for Endocrinology, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK; 2Fetal Medicine Unit, Royal London Hospital, London, UK.


Background: Delta-like homologue 1 (DLK1) encodes a transmembrane protein, which may also be secreted into the circulation. Levels are known to rise in maternal serum during late gestation and our genetic studies in the mouse have shown that this DLK1 arises from the conceptus. The cell population that secretes DLK1 into the maternal circulation has not been identified. In humans DLK1 has been shown to be differentially expressed in intrauterine growth restricted (IUGR) when compared with normal placentas suggesting a role in intrauterine growth.

Objective and hypothesis: We hypothesise that maternal serum levels of DLK1 derived from the conceptus may reflect indices of fetal and placental growth. Our objective is to find the source population of DLK1-secreting cells in the placenta, and assess if maternal circulating DLK1 correlates with fetal growth parameters.

Methods: 45 women from our Obstetric Department were followed up prospectively. Measurements of fetal growth parameters, maternal serum samples (for DLK1 ELISA) and clinical data were collected at 20, 28, 34, and 38 weeks gestation. DLK1 immunohistochemistry was carried out on placental samples.

Results: We localised DLK1 expression to cell populations within the placental villi including the fetal endothelium and trophoblast compartments. Maternal DLK1 levels rise during gestation and fall post-delivery. Furthermore there was a positive correlation between DLK1 levels from ~32 weeks and birth weight. DLK1 serum levels were also lower in our IUGR population.

Conclusion: Fetal endothelium and trophoblast cell types of the placenta express DLK1 and may be responsible for its secretion into the maternal circulation. DLK1 levels positively correlate with normal fetal growth in the 3rd trimester and low DLK1 levels are associated with poor fetal growth. DLK1 may be a novel endocrine marker of human fetal growth.

Volume 36

42nd Meeting of the British Society for Paediatric Endocrinology and Diabetes

British Society for Paediatric Endocrinology and Diabetes 

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