Smoking and preterm birth: mechanisms and consequences

Smoking is known to increase the risk of both spontaneous and elective preterm birth, but the association with spontaneous preterm birth is stronger. There are many potential pathways through which smoking may cause premature labour. These include nicotine-induced vasoconstriction, carbon monoxide-induced fetal hypoxia, cadmium disruption of calcium signalling, altered steroid hormone production, changed responses to oxytocin and altered prostaglandin production and metabolism.
This project will examine the impact of smoking on protein expression in placenta, fetal membranes and decidua, focussing on the inducible prostaglandin synthase PTGS2 and 15-hydroxy prostaglandin dehydrogenase (HPGD). The consequences of PTGS2/HPGD alterations will be assessed by measuring prostaglandins and a wide range of metabolites under basal conditions and after stimulation with oxytocin, inflammatory cytokines and growth factors.
Uterine tissues will be obtained with ethical approval and informed consent from women delivering at St Michael’s Hospital, Bristol. Laboratory work will be based at the Dorothy Hodgkin Building. The data will provide insight into how smoking can lead to pregnancy complications.