We specialise in medical, biological, health and social care sciences. We currently have over 250 students in programmes engaged in research. The Research Excellence Framework (REF), a new national assessment of research at UK universities has ranked St George’s, University of London, as fourth for impact of its research on the global community.

HIV research

We offer a number of programmes with wide-ranging opportunities for translational research. We offer PhD study opportunities as well as MPhil, MD(Res) and a number of our taught Master's courses includes a research project. A core training course for research students supports the acquisition of more generic research skills and provides opportunities for peer-group support.

Read more about research degrees at St George's

Currently Available Studentships

The following Vascular Biology MPhil/PhD students are currently available at St George's.  Two full time studentships are available, with a stipend paid at MRC rates and fees paid for a period of three years. 

To apply for (up to two) of these projects you should complete the application form and send the reference form to your referees.  The closing date for receipt of both application and references is 17:00 on Monday 15 October.  If you wish to make further enquiries about the project, then there is an email link to the Lead Supervisor for each project.  Applications and references should be submitted to This email address is being protected from spambots. You need JavaScript enabled to view it.

Application Form

Reference Form

Supervisory team

Project title Project details Training and skills

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Professor J Cartwright

Professor G Whitley

The interaction between the maternal-fetal interface,the uteroplacental circulation and maternal haemodynamics in preeclampsia and fetal growth restriction

Pre-eclampsia is a pregnancy complication characterised by high maternal blood pressure and protein in the urine. It is often associated with fetal growth restriction and is one of the most common causes of maternal and fetal mortality. This project will explore the interactions that occur at maternal-fetal interface between the placenta and the maternal cardiovascular system in pregnancies complicated by preeclampsia and fetal growth restriction.

Pregnancy is associated with marked maternal haemodynamic changes. Preeclampsia is a pregnancy complication characterised by high blood pressure and elevated protein in the urine. It is often associated with fetal growth restriction and is one of the most common cause of maternal and fetal mortality.  Preeclampsia and fetal growth restriction result from impaired trophoblast invasion and resulting placental insufficiency. Women who develop preeclampsia are likely to have pre-pregnancy cardiovascular predisposition and are known to have a long-term risk of hypertension, coronary heart disease and stroke later in life. The reason why some women develop preeclampsia with fetal growth restriction, preeclampsia without growth restriction or growth restriction without preeclampsia is yet to be established.

The aim of this study is to explore the interactions between factors released by the placenta and the maternal cardiovascular system. The haemodynamics will be determined in 4 groups of pregnancies: those complicated by preeclampsia and fetal growth restriction, preeclampsia without growth restriction, fetal growth restriction without preeclampsia, and normotensive controls with appropriately grown fetuses. Assessment will be made of the uteroplacental circulation using uterine artery Doppler and shear wave elastography of the placenta, while maternal haemodynamics will be assessed by recording of the arterial stiffness using arteriography, and maternal cardiac function. Results will be correlated with circulating concentrations of novel factors secreted by the placenta. The direct effect of these factors on isolated uterine vessels and maternal endothelial cells will be determined. At delivery, samples from the placenta and uterine biopsies will be taken to assess the maternal-fetal interface, including spiral artery remodelling. The findings and their interactions will be compared in the 4 study groups.
  • Laboratory skills: Cell and Molecular Biology
  • Cardiovascular imaging, such as ultrasound assessment of the placental shear wave elastography and Doppler
  • Non-invasive assessment of maternal haemodynamics, including arterial stiffness, cardiac output and systemic vascular resistance
  • Critical appraisal of the literature and of the research findings
  • Statistical analysis of scientific quantitative data

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Professor A Albert     
Regulation of Kv7 channels by myristoylated alanine-rich C kinase substrate (MARCKS) in rat and human arteries

Kv7 channels are important determinants of arterial smooth muscle contractility in rodent and human arteries, and dysfunction of these channels has been implicated in vascular disease. Identifying how Kv7 channels are regulated will improve our understanding of vascular disease and open up new avenues for therapeutic intervention. Kv7 channel activity is reliant upon phosphatidylinositol 4,5-bisphosphate (PIP2) and we recently discovered that myristoylated alanine-rich C kinase substrate (MARCKS), a PIP2-binding protein, influences arterial contractility. The aim of this studentship is to characterize the interactions between Kv7 channels, PIP2 and MARCKS in normotensive and hypertensive rats, and in human arteries from patients undergoing elective surgery.

Extensive research has shown Kv7 channels are important for keeping arteries relaxed and allowing them to respond to receptor-mediated vasorelaxants. PIP2 is necessary to maintain Kv7 channel activity and we have recently showed that myristoylated alanine-rich C kinase substrate (MARCKS) regulates local PIP2 levels in arteries. The goal of the studentship is to characterize the relationship between the three Kv7 isoforms expressed in vascular smooth muscle cells (Kv7.1, 7.4, 7.5) and MARCKS in different arteries from Wistar rats as well as human arteries received from elective surgery. We will use immunocytochemistry to define the expression of MARCKS and Kv7 proteins in smooth muscle cells from rat mesenteric, coronary and cerebral arteries and will define interactions between MARCKS and Kv7 proteins by proximity ligation assay. The functional effect of MARCKS-Kv7 interaction will be quantified using single cell electrophysiology and whole artery myography. We will ascertain how Kv7 activators relax the different arteries when MARCKS/PIP2 association is disrupted by a competitive peptide, MANS. Membrane PIP2 will be assayed using reporter molecules provided by collaborators. We will also characterize the contribution of Kv7 channels to receptor-mediated relaxations in the absence and presence of MANS or following morpholino-derived knockdown of MARCKS.

The project will provide excellent training in modern vascular research techniques and science dissemination within a vibrant, multi-disciplinary environment.
The student will receive comprehensive training in modern vascular research techniques including whole artery myography, single cell electrophysiology, immunocytochemistry, confocal microscopy, proximity ligation assay, and molecular interference by morpholino and adenoviral transfection. Presentation of work at national and international meetings, and visits to other laboratories is actively encouraged

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Dr I Dumitriu
Macrophages as regulators of placental development in pregnancy

A successful pregnancy outcome for both mother and baby is dependent on normal placental development and function. As the placenta grows new blood vessels develop in a tightly controlled manner. Placental macrophages (Hofbauer cells) are found in larger numbers in early pregnancy and although they are found in close proximity to the developing vessels and their function in regulating normal angiogenesis and therefore placental development has been little studied. This project will examine the role these macrophages have in normal pregnancies and those pregnancies at higher risk of serious complications such as pre-eclampsia and fetal growth restriction, where placentation is impaired. 

A successful pregnancy outcome for both mother and baby is dependent on normal placental development and function. Poor placentation is commonly associated with diseases such as fetal growth restriction (FGR) and preeclampsia (PE). FGR, where a baby fails to reach its genetically determined growth potential, affects 5–8% of human pregnancies worldwide and is a major cause of neonatal morbidity and mortality. Two processes control the growth of the placenta and therefore growth of the fetus. The first is the expansion of the trophoblastic epithelium and the second is the growth of the placental vasculature by angiogenesis. FGR is associated with alterations in both trophoblast differentiation and placental angiogenesis. Fetal macrophages (Hofbauer cells) are present in close proximity to the developing vessels and are likely to play a key role in regulating placental development.

Understanding, and ultimately treating, the pathology of FGR/PE will require an increase in our knowledge of the complex interactions occurring in a normal pregnancy and comparing these to compromised pregnancies. Measurement of uterine artery resistance indices by Doppler Ultrasound in the first trimester can be used to identify pregnancies at an increased risk of developing FGR/PE. The aim of this study is to compare first trimester placental macrophages isolated from pregnancies screened, prior to termination of pregnancy, as being at the highest and lowest risk of developing FGR/PE, had the pregnancy progressed. It is our hypothesis that first trimester placental macrophages influence the behaviour of endothelial cells. Additionally we hypothesise that macrophages from pregnancies with a higher risk of developing FGR/PE have altered secretion of cytokines, pro- and anti-angiogenic factors, and are less able to promote angiogenesis.
Isolation and culture of cells from the first trimester placenta. Characterisation of receptors (flow cytometry and immunohistochemistry), secreted factors (multiplex arrays, ELISAs). Functional co-culture studies to determine regulation of angiogenesis, endothelial cell biology using 3D cultures, time-lapse and confocal microscopy.

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Dr N Anim-Nyame
The role of the microcirculation in the pathogenesis of hypertension and cardiovascular disease in women with a history of a hypertensive disorder of pregnancy or preeclampsia

Preeclampsia is a pregnancy specific disorder characterised by hypertension and proteinuria. Women with a history of preeclampsia are at increased risk of hypertension, stroke, and cardiovascular mortality in later life. The mechanism(s) by which these disorders are associated with preeclampsia are not fully understood, but impaired tissue perfusion and small blood vessels abnormalities including a reduction in capillary density or “capillary rarefaction” (CR) have been implicated in the pathogenesis.  We have recently reported that women who later on developed preeclampsia had significant structural CR early in their pregnancy before the onset of preeclampsia. We also found that significant CR persisted in the post-partum period and did not recover to levels observed in normal pregnancy suggesting that CR may be involved in long term hypertension and cardiovascular risk.

Women with pre-eclampsia (PE) undergo significant heart remodelling, and a significant percentage of these women demonstrate marked myocardial damage and diastolic dysfunction. There is increasing evidence of widespread microcirculatory and endothelial cell abnormalities in PE. We recently reported for the first time that women who later on developed PE had significant structural CR early in their pregnancy before the onset of PE. We also found that significant CR persisted in the post-partum period and did not recover or reverse back to early pregnancy levels or to levels observed in normal pregnancy suggesting that CR may be involved in long term hypertension and cardiovascular risk. There is accumulating evidence that CR represent an independent form of structural microvascular disease with potential clinical consequences. In patients with dilated cardiomyopathy and congestive heart failure, analysis of endomyocardial biopsy specimens revealed marked CR associated with a reduced coronary blood flow reserve.

Aims and Objectives:

1)To assess myocardial microvascular perfusion and oxygen consumption in women with a history of pre-eclampsia using Blood Oxygen Level-Dependent (BOLD) Cardiovascular Magnetic Resonance (CMR)

2)To assess skin capillary microcirculation using intravital capillary microscopy and correlate the degree of capillary rarefaction with CMR measures.

Intravital capillary measurements (Capillaroscopy): Capillaroscopy will be performed using the iCAPPPs machine. The number of capillaries will be counted on-line using computer software (KK-Technology, England). Room temperatures will be monitored.

Blood Pressure Measurement:
Sitting blood pressure will be measured using an automatic oscillometric sphygmomanometer (Omron) with an appropriate cuff size. Three sitting BP measurements will be taken and the average of the last 2 readings will be recorded as the average.

Central BP Measurement & Aortic Augmentation Index
This will be measured using the Omron HEM-9000AI device (Omron Healthcare, Kyoto, Japan) 15. Radial artery tonometry will be performed on the left arm of each participant, and blood pressure will be measured simultaneously in the right arm using the BP cuff of the Omron HEM-9000AI device just prior to central pressure assessment. The quality of the recordings will be assured by discarding all the recordings with an error message.

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Professor G Whitley

Dysfunctional endothelial cells and heart failure: is NOX1 a potential therapeutic target?

Cardiac endothelial cell (EC) dysfunction is the underlying feature of diastolic-heart failure and agents that improve EC function are urgently needed. My preliminary findings show that the oxidative stress-inducing NADPH oxidase NOX1 causes pulmonary EC dysfunction and selective NOX1 inhibitors can restore function. This project will investigate cardiac endothelial NOX1 and ascertain whether this is a therapeutic target for heart failure. Specifically, we will characterise NOX1 in terms of angiogenic signalling and the consequent functional effects on cardiac ECs using (i) in vitro cell models, (ii) ex vivo organo-culture systems, and (iii) an in vivo murine heart failure model.

Dysfunctional cardiac endothelial cells (ECs) are the underlying cause of diastolic-heart failure (HF), a debilitating condition with high morbidity and mortality. Diastolic-HF patients typically co-present with coronary artery and/or peripheral vascular diseases, where increased EC apoptosis, EC-to-fibroblast transformation, and perturbed angiogenesis (endothelial sprouting/proliferation) are shared aetiological features. Underpinning these dysfunctional EC responses is oxidative stress, one source of which is the family of NADPH oxidases (NOXs). My previous work showed that matricellular proteins regulate NOX1, which subsequently perturbs pulmonary EC function. Recent unpublished data indicate that hypertensive agents increase matricellular protein and NOX1 expression in the heart; however, whether this affects cardiac EC function is unknown. Therefore, the hypothesis for this studentship is that NOX1 dysregulation in cardiac ECs is a primary cause of heart failure.  Here, we will use coronary microvascular ECs treated with different matricellular proteins. To determine the role of NOX1 in cellular responses, gene knockdown (e.g. Crispr-Cas9) or inhibitor strategies will be used. Effects on oxidative stress-dependent protein kinase signalling and gene expression will be assessed by immunoblotting and qPCR, with functional EC readouts (e.g. proliferation or in vitro wound scratch assay) assessed using standard methods. To assess NOX1 in cardiac angiogenesis, ex vivo heart samples in a 3D-matrix assay will be used in combination with selective NOX1 inhibitors. Finally, NOX1 inhibition in hypertension-induced cardiac dysfunction will be assessed in vivoThis project will establish the role of NOX1 in cardiac ECs and identify NOX1 as a potential therapeutic target for HF.

Training in the following techniques will be provided:

In vitro EC and ex vivo organo-cultures to explore EC physiology

Immunoblotting and immunostaining

RNA preparation and quantitative PCR techniques

Confocal Microscopy

siRNA/Crispr-Cas9

Rodent handling and tissue harvesting.

Histology

Skills to be developed include:

Design and conduct of scientific experiments.

Statistical evaluation of data.

In-depth understanding of oxidative stress signalling.

Presentation of scientific data.

Time-management and organisational abilities.

Management of written records and cross-referencing of electronic data files.

Use of computer software for research.

Finally, the student will be expected to take advantage of training courses offered by the graduate school.

Last Updated: Friday, 14 September 2018 15:01