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Department of Physiology, Development and Neuroscience


Graham Burton qualified in medicine from the Universities of Cambridge and Oxford, but returned to pursue basic research at Cambridge, where he held the Mary Marshall and Arthur Walton Professorship of the Physiology of Reproduction until his retirement in 2020. He has a long-standing interest in early placental development and function, and in particular how this is influenced by the prevailing oxygen concentration. In collaboration with Eric Jauniaux, he showed the importance of the uterine secretions in supporting development of the human embryo during the first three months of pregnancy before the maternal circulation to the placenta is fully established. Most recently, he has been involved in the derivation of both endometrial and trophoblast organoids, allowing the maternal-fetal interactions during early pregnancy to be investigated in a systematic fashion.

His research has been acknowledged by the award of several international prizes, including the FEDERA award from the Dutch Federation of Medical Scientific Societies, the Anne McLaren Distinguished Scientist Award from the Society for Reproduction and Fertility, and the Joan Hunt Senior Award in Placentology from the International Federation of Placenta Associations. He was elected a Fellow of the UK Academy of Medical Sciences in 2011, and of the Royal Society in 2022. He was the Founding Director of the Centre for Trophoblast Research, a centre-of-excellence in placental biology, at the University of Cambridge in 2007, and was the founder and inaugural Chair of a cross-disciplinary Strategic Research Initiative on Reproduction at the University that brings together the biological, clinical and social sciences with the arts and humanities. He has published over 250 peer-reviewed articles, authored and edited 4 books, and written over 30 book chapters. He has an H-score of 97 (Google scholar).  


Our focus is on human placental development, and the involvement of the placenta in complications of pregnancy such as miscarriage, fetal growth restriction and pre-eclampsia. In particular, we are interested in the effects of oxygen, hypoxia, and oxidative and endoplasmic reticulum stress on trophoblast differentiation and function. This interest stems from our finding, in collaboration with Professor Eric Jauniaux, that the maternal arterial circulation to the placenta is not fully established until towards the end of the first trimester of pregnancy. We demonstrated that prior to this time the conceptus is supported by secretions from the endometrial glands, histotrophic nutrition, that are delivered into the intervillous space through the developing basal plate. Consequently early development takes place in a physiologically low oxygen environment, and there is a threefold increase in the intraplacental oxygen concentration at the start of the second trimester, the oxygen transition. Currently, we are investigating how the placenta may stimulate its own development during early pregnancy by signalling to the endometrial glands and upregulating their secretion of growth factors and nutrients.

Our research has shown that fluctuations in oxygenation are particularly damaging to the trophoblast, leading us to propose ischaemia-reperfusion as the primary placental insult when trophoblast invasion and spiral artery remodeling are deficient. Recent work has elucidated the 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, describing a spectrum of changes from homeostatic adaptations to low oxygen in healthy high-altitude pregnancies to frank pathology in cases of fetal growth restriction. Most recently, we have shown that the placental molecular pathology is strikingly different in cases of early-onset pre-eclampsia compared to late-onset cases, demonstrating that the syndrome is heterogeneous and has different aetiologies.

Key advances of the group since 2010

2010: Identified a transcriptional network that may define a trophoblast stem cell population within the placenta

2011: Identified that soluble FLT1 sensitises endothelial cells to pro-inflammatory cytokines, a potential mechanism in pre-eclampsia

2012: First demonstration that endoplasmic reticulum stress compromises mitochondrial function through inhibition of synthesis of MTC complexes

2013: First demonstration that hydrogen sulphide is a potent placental vasodilator, and that production is impaired in pathological placentas with increased vascular resistance

2014: First demonstration of the heterogeneity of placental molecular pathology in pre-eclampsia

2015: Identified that different epigenetic states define syncytiotrophoblast and cytotrophoblast nuclei in the trophoblast

2016: Computational modeling of oxygen exchange across terminal villi of the human placenta

2017: First derivation of hormone-responsive organoid cultures of human endometrium; First RNA-Seq of the human yolk sac showing conservation of functions

Funding: MRC, Wellcome Trust Programme grants, Anatomical Society, Action Medical Research, Evelyn Trust


Professor Eric Jauniaux (University College Hospital, London)
Professor Stephen Charnock-Jones (University of Cambridge)

Professor Anne Ferguson-Smith (University of Cambridge)
Professor Ashley Moffett (University of Cambridge)
Dr Andrew Murray (University of Cambridge)
Dr Myriam Hemberger (Braham Institute)

Professor John Kingdom (University of Toronto)
Dr Hong wa Yung (Senior Research Associate)
Dr Tereza Cindrova-Davies (Research Associate)
Ms Nadia Capatina (Graduate Student)


Key publications: 

Cindrova-Davies T, Jauniaux E, Elliot MG, Gong S, Burton GJ, Charnock-Jones DS, (2017), RNA-seq reveals conservation of function among the yolk sacs of human, mouse, and chicken, Proc Natl Acad Sci U S A;114(24):E4753-E61

Turco MY, Gardner L, Hughes J, Cindrova-Davies T, Gomez MJ, Farrell L, et al, (2017), Long-term, hormone-responsive organoid cultures of human endometrium in a chemically defined medium, Nat Cell Biol;19(5):568-77

Burton GJ, Fowden AL, Thornburg KL, (2016), Placental Origins of Chronic Disease, Physiol Rev;96(4):1509-65

Burton GJ, Jauniaux E, (2105), What is the placenta? Am J Obstet Gynecol;213(4 Suppl):S6 e1, S6-8

Fogarty NME, Burton GJ, Ferguson-Smith AC, (2015), Different epigenetic states define syncytiotrophoblast and cytotrophoblast nuclei in the trophoblast of the human placenta, Placenta, 36, 796-802

Burton GJ, Fowden AL, (2015), The placenta; a multifaceted, transient organ, Philosophical Transactions of the Royal Society B, 370, 21040066

Yung HW, Atkinson D, Campion-Smith T, Olovsson M, Charnock-Jones DS, Burton GJ, (2014), Differential activation of placental Unfolded Protein Response pathways implies heterogeneity of causation of early- and late-onset pre-eclampsia, Journal of Pathology, 234, 262-276

Cindrova-Davies T, Herrera EA, Niu Y, Kingdom J, Giussani DA, Burton GJ, (2013), Reduced cystathionine g-lyase and increased miR-21 are associated with increased vascular resistance in growth-restricted pregnancies: hydrogen sulfide as a placental vasodilator, American Journal of Pathology, 182, 1448-1458

Benirschke K, Burton GJ, Baergen R, (2012), Pathology of the Human Placenta, 6th edition, Springer, Berlin, pp. 941


Full list of publications

Emeritus Mary Marshall and Arthur Walton Professor of the Physiology of Reproduction (retired)
Founding Director of Centre for Trophoblast Research
 Graham  Burton

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