Rebecca Jones

Overview

I am a Senior Lecturer in Maternal and Fetal Health and am based in the Maternal and Fetal Health Research Centre, in St Mary's Hospital.

I head a research programme investigating the causes of pregnancy complications, with a particular interest on immunological mechanisms of pregnancy pathologies and maternal influences on fetal and placental growth.

I am the Co-Director of the Masters in Research (MRes) in Maternal and Fetal Health, and currently supervise 1 MRes and 5 PhD students.

I am Postgraduate Research Student Trainer for the Institute of Human Development

I am also involved in undergraduate teaching, both for the Faculty of Medical and Human Sciences and for the Faculty of Life Sciences.

Biography

My previous research, both during my PhD in Edinburgh and postdoctoral training in Melbourne, focused on inflammatory processes involved in regulating normal endometrial function, and how these are aberrant in endometrial pathologies, e.g. infertility, abnormal uterine bleeding, endometrial cancer. These studies gave me a strong foundation in basic science and clinically-relevant research in Obstetrics and Gynaecology. In 2002 I was awarded a Fellowship from the Australian and New Zealand Royal College of Obstetricians and Gynaecologists. This provided me with the opportunity to develop research independence and head my own research group. I employed a research assistant and supervised undergraduate students and co-supervised a PhD student. This fellowship, and additional travel grant awards, enabled annual travel to international meetings, predominantly in the USA, to raise my international research profile.

My current research focuses on maternal and fetal interactions during pregnancy. I was originally employed in 2005 at the University of Manchester as a link lecturer with Professor John Challis at the University of Toronto, with a brief to bring together research projects in Manchester and Toronto on the theme of developmental programming. I have therefore developed a portfolio of research projects to examine how the maternal environment shapes the development and function of the placenta, and thereby affects the health and timely delivery of the infant.
Many pregnancy pathologies have their origins in early pregnancy, and my previous research has contributed to our understanding of the essential preparatory events within uterine decidua for embryo implantation and placentation. One particular focus has been investigating the regulation and functions of immune cells in regulating uterine physiology. Together with collaboration with researchers at the University of Toronto, my group has shown for the first time that maternal immune cells play an integral role in the remodelling of the uterine arteries during early pregnancy, an essential preparatory event for a healthy pregnancy. We have also delineated key roles for maternal macrophages within the decidua in later pregnancy during the labour process both at term and in preterm deliveries. This is coincident with the upregulation of a number of chemoattractants which we believe participate in triggering labour and thus may be harnessed to block premature labour. The presence of these cytokines in maternal plasma may provide a more accurate means of identifying those women in imminent risk of preterm delivery enabling targeting of interventions to those most at need.

Since taking up my post in Manchester, I have also broadened my research focus to include investigations of the impact of maternal nutritional status and stress on placental development and function. These are major influences on fetal growth and developmental programming and our work explores the mechanisms involved in glucocorticoid-mediated growth restriction using animal models and human placental tissue. Much of the research into nutritional status revolves around teenage pregnancy, due to their increased risk of poor pregnancy outcome and their susceptibility for low nutritional status. We have shown that teenagers have inherently low placental function, confirming a biological susceptibility related to young maternal age. This is exacerbated in those teenagers with poor nutritional status and we are exploring epigenetic mechanisms. We are now extending these studies to examine the effect of advanced maternal age, as older mothers are also more likely to suffer pregnancy complications, particularly stillbirth. This provides the opportunity for more clinically-relevant research with clear translational potential.