Professor Graham Burton
- Mary Marshall and Arthur Walton Professor of the Physiology of Reproduction (retired)
- Director of Loke Centre for Trophoblast Research (Retired)
- Royal Society Fellow
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About
Graham Burton is a reproductive biologist recognised for his research into the development of the human placenta. Initially trained in medicine at the Universities of Cambridge and Oxford, he pursued basic research at Cambridge where he is Mary Marshall and Arthur Walton Professor Emeritus of the Physiology of Reproduction. His team identified that the human placenta initially develops in a protective low-oxygen environment supported by the secretory lining of the uterus. Only once the embryo's major organ systems have differentiated does the placenta gain a blood supply from the mother. Graham has also shown how aberrations in establishing the placenta lead to later complications of pregnancy, ranging from miscarriage to pre-eclampsia.
Graham's contributions have been recognised by several international prizes, including the FEDERA award from the Dutch Federation of Medical Scientific Societies and the Anne McLaren Distinguished Scientist Award from the Society for Reproduction and Fertility. He was elected Fellow of the Academy of Medical Sciences in 2011, and elected Fellow of the Royal Society in 2022. He was founding Director of the Loke Centre for Trophoblast Research at the University of Cambridge.
Research
Research summary
Our focus is on human placental development, and the involvement of the placenta in complications of pregnancy such as miscarriage, intrauterine growth restriction and pre-eclampsia. In particular, we are interested in the effects of oxygen, hypoxia and oxidative stress on trophoblast differentiation and function. This interest stems from our finding, in collaboration with Eric Jauniaux, that there is a threefold increase in the oxygen concentration at the end of the first trimester as a result of the onset of the maternal arterial circulation to the placenta. We have demonstrated that prior to this time the embryo is supported by secretions from the endometrial glands.
Our research has shown that fluctuations in oxygenation are particularly damaging to the trophoblast. Recent work has elucidated signalling pathways activated by that stress, leading to changes in gene transcript profiles and cytokine secretion that may stimulate the development of pre-eclampsia. We have also provided the first evidence that the syncytiotrophoblast is vulnerable to endoplasmic reticulum stress, and that this plays a major role in the pathophysiology of the reduced placental growth and endocrine activity seen in cases of intrauterine growth restriction. We are currently investigating how this impaired placental function may affect developmental programming of the fetus.
We have a number of highly productive collaborations both within and outside the Centre.
Funding: Wellcome Trust Programme grant, Anatomical Society, Action Medical Research, MRC, Evelyn Trust