Miss Christina Hayward PhD.


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I graduated with a BSc (Hons) in Medical Molecular Biology from Cardiff University and obtained a PhD at the University of Manchester in the Maternal and Fetal Health Research Group. Supervised by Dr Rebecca Jones and Dr Susan Greenwood and funded by Action Medical Research, my PhD project investigated the influence of continued maternal growth on placental growth, development and function in teenage pregnancies. Teenagers are susceptible to delivering small-for-gestational-age (SGA) or growth restricted babies. These pregnancy outcomes are associated with perinatal mortality and morbidity, and an increased risk of chronic health problems in later life, including cardiovascular disease, obesity and diabetes.  Previous studies implicated young maternal age and continued skeletal growth as potential influencing factors in teenage pregnancy. My PhD focused on delineating the mechanisms underlying teenagers' susceptibility to SGA birth. My studies, which followed on from the About Teenage Eating study (PIs Professors Philip Baker and Lucilla Poston), demonstrated that placental nutrient transport capacity was inherently reduced in teenagers compared to adults; however, pregnant teenagers who continued to grow were able to compensate by up-regulating amino acid transport across the placenta, and consequently delivered larger babies. These studies also indicated that growing teenagers may have a maternal hormonal milieu that is conducive to fetal growth by stimulating nutrient transport.

My first postdoctoral research associate position was funded by the British Heart Foundation working with Dr Mark Wareing, Mrs Elizabeth Cowley, Dr Tracey Mills and Professor Colin Sibley. The project investigated whether the increased incidence of pre-eclampsia in women with raised body mass index (BMI) is associated with altered omental fat adipokine secretion and promotion of maternal vascular endothelial dysfunction. We demonstrated that obese (BMI ≥30kg/m2) pregnant women have impaired myometrial artery function suggested to be thromboxane and/or nitric oxide pathway specific. In comparison to normal-weight (BMI 18-24kg/m2) pregnant women, omental (central) fat tissue from obese pregnant women produced altered concentrations of adipokines, namely leptin and adiponectin. We suggested that an aberrant endocrine environment created by increased central adiposity induces vascular endothelial dysregulation in obese mothers, which may predispose them to pre-eclampsia.

My second postdoctoral position was funded by the Medical Research Council working with Dr Mark Dilworth investigating placental adaptations and their role in maintaining normal fetal growth. Placental dysfunction is a major cause of fetal growth restriction (FGR), the inability of a fetus to achieve its genetic growth potential. FGR is a serious complication of pregnancy for which there is currently no therapy. This emphasises the need for better understanding of how fetal growth is normally achieved and how it is dysregulated in FGR. Adequate nutrient delivery from mother to baby is essential for optimal fetal growth. We examined how placental nutrient transport can be altered to meet the needs of the developing fetus and how these adaptations may be regulated by fetal signals. We investigated whether failure of placental adaptive responses contribute to the development of FGR.

My current postdoctoral position with Professor Martin Schwartz in the Wellcome Trust Centre for Cell Matrix Research focuses on the regulation of fibroblast extracellular matrix (ECM) synthesis in the heart. Cardiac fibroblasts (CFs) are responsible for ECM homeostasis in health and its deposition and remodelling post-injury (e.g. myocardial infarction). Initially, ECM deposition is a protective mechanism needed for wound healing and tissue regeneration but excessive and continuous ECM production, known as fibrosis, results in compromised heart function and ultimately heart failure. Therapies are needed for preventing excessive ECM production without altering normal repair, thus, understanding the CF contribution to fibrotic disease progression will aid therapeutic strategies. Using matrix-based 3D cell culture, we are investigating the underlying mechanisms of homeostatic fibroblast ECM production and the potential role that inflammatory factors, hypoxia and/or cell polarity have to play in cardiac fibrosis. 


PhD Medicine
The University of Manchester, UK

BSc (Hons) Medical Molecular Biology
Cardiff University, UK

Memberships of committees and professional bodies

International Federation of Placenta Associations

The Physiological Society

Society of Endocrinology

Sustainable Development Goals

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