PhD opportunities

Information about available funded PhD Positions

Molecular signalling underlying blood development in engineered AGM organoids

Application Deadline: February 27, 2026

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Supervisors: Prof. Alexander Medvisnky (The University of Edinburgh), Dr. Guillaume Blin (The University of Edinburgh)

About the Project

Haematopoietic stem cells (HSCs) are broadly used for clinical transplantations, but their supply is insufficient to meet clinical demand. During embryo development, HSCs emerge in the aorta-gonad-mesonephros (AGM) region through the process called endothelial-to-haematopoietic transition (EHT), which can be recapitulated in mouse AGM cultures. However, derivation of clinically relevant human HSC from ES/iPS cells remains a challenge, mainly due to poor understanding of mechanism underlying this process. 

Hypothesis and goals. 

During embryogenesis, organs and tissues show a great degree of self-organisation. Physical constraints can be a major contributor to tissue patterning and cell specification. The main objective of the project is to engineer a human ESC-based AGM organoid system to investigate effects of spatial constraints and dorso-ventral molecular polarisation on EHT, ultimately revealing a pathway for generation of HSCs.

Approaches and methodology. We will model EHT in vitro in highly controllable spatiotemporal conditions using fluorescent reporter hESC lines to track EHT using live imaging. Geometrically constrained supports for cultured cells and polarised signalling will be engineered using cutting-edge micropatterning machine. Confocal microscopy, flow cytometry, gene expression analysis as well as molecular perturbations will be employed for efficient mechanistic analyses of EHT. 

Training. The student will receive interdisciplinary training in areas of microfabrication, developmental biology, experimental haematology, gene editing (CrispR/CAS9), flow cytometry, confocal microscopy and bioinformatics. 

Impact.  Pluripotent hES/iPS cells hold great hope for regenerative medicine. Generation of HSCs from hES/iPS cells could overcome the shortage of donors and enhance efficiency of clinical transplantation for treatment of haematopoietic disorders including blood cancers. This project can help develop new protocols for directed differentiation of bona fide HSCs for clinical applications. 

Environment. We have shown the central role of AGM region in HSC development and demonstrated its autonomous capacity to generate HSCs in culture. We have strong record of studying spatial aspects of mouse and human AGM regions at cellular and molecular levels. The project will benefit from expertise of additional supervisors: Dr. Guillaume Blin, Quantitative Biology of Pattern Formation group (SBS) and Prof. Denis Headon, Vertebrate Developmental Biology (Roslin Institute).

For more information on the project, eligibility and how to apply for the School's PhD programme, please follow this LINK.

Applicants should apply to either the School's (a) Biological Sciences PhD programme or (b) Biological Science with Internship PhD programme via the University’s admissions portal (EUCLID) with a start date of 01 October 2026.

In the EUCLID application, applicants should state the project “Molecular signalling underlying blood development in engineered AGM organoids”, the research supervisor (Alexander Medvinsky) and their anticipated funding source (e.g. EPSRC DLA School studentship)


Funding Notes

This project will be funded by an EPSRC Doctoral Landscape Award (DLA) studentship via the College of Science and Engineering. 

Only UK/Home eligible students are eligible for this funding allocation. Applicants eligible for the studentship and who apply to this project will automatically be considered for this funding award. 

The studentship provides cover for an annual stipend (£20,780 in 25/26 AY) and Home level tuition fees (£5006 in 26/26 AY).  Funding to support project delivery and professional development opportunities will be provided by the recruiting supervisor.


References

Medvinsky, A. and Dzierzak, E. (1996). “Definitive hematopoiesis is autonomously initiated by the AGM region”. Cell 86, pp.897-906
C. Souilhol, C. Gonneau, J. G. Lendinez, A. Batsivari, S. Rybtsov, H. Wilson, D. Hills, S. Taoudi, J. Antonchuk, S. Zhao, A. Medvinsky (2016) “Inductive interactions mediated by interplay of asymmetric signalling underlie development of adult haematopoietic stem cells. Nat. Commun. 7, 10784.
E. I. Crosse, S. Gordon-Keylock1, S. Rybtsov, A. Binagui-Casas1, H. Felchle, K. Kirschner, N. Nnadi, T. Chandra, S. Tamagno, D. J. Webb, F. Rossi, R. A. Anderson, A. Medvinsky (2020). Multi-layered spatial transcriptomics identify secretory factors promoting human hematopoietic stem cell development. Cell Stem Cell 27, 822-839.

Contact details

For more information, please contact Prof. Alexander Medvinsky A.Medvinsky@ed.ac.uk

 

 

Evaluating the systemic effect of myocardial infarction on bone marrow hematopoiesis and organ fibrosis to inform drug development

Closed for Applications

Supervisors: Dr Mihaela Crisan (The University of Edinburgh), Dr Cecile Benezech (The University of Edinburgh)

About the Project

This 3-year, fully-funded PhD studentship is established with a generous donation from the Mary Kinross Charitable Trust to the Institute for Regeneration and Repair (IRR), a research institute based at the University of Edinburgh. Scientists and clinicians at IRR study tissue regeneration and repair to advance human health and reproductive outcomes. The Institute incorporates three leading research centres with a focus on regenerative medicine, inflammation and reproductive health.

Summary

Cardiovascular diseases, including heart attack, are the leading cause of death globally. Timely treatment of a heart attack by emergency medical services and hospitals has the potential to prevent multi-organ failure and death. This PhD project aims to develop treatments for heart attacks by studying (i) how blood vessels respond to heart injury and (ii) how the disease spreads to other organs. The project will be carried out at the Institute for Regeneration and Repair, and will use novel technologies to identify key cells and mechanisms involved in the disease process, to identify potential targets for drugs to improve patient outcomes.

Project outline

Cardiovascular disease, a group of disorders affecting the heart and blood vessels, remains the leading cause of mortality worldwide. Cardiac fibrosis represents a major pathological feature contributing to nearly all types of heart disease.1 It plays a key role in the development of heart failure and is often initiated after myocardial infarction (MI).2 Blood vessels are central to the progression of cardiac fibrosis. After injury, the cells which are in direct contact with the endothelium, called pericytes detach from blood vessels, and migrate towards the wound to deposit collagen. We and others found that the transmembrane receptor CD248 is upregulated on pericytes after MI and contributes to inflammation and fibrogenesis in the heart.

Recent studies have shown that MI leads to significant bone marrow remodelling.4 This suggests a change in the hematopoietic supportive niche, including pericytes5, which could be contributing to increased long term systemic inflammation after MI and propagation of fibrosis to other vital organs as well, including kidneys, liver, and lung.6

Our hypothesis is that pericytes and CD248 play a central role in the propagation of systemic fibrosis, post-MI. We propose that blocking CD248 action may protect against BM remodeling and the perpetuation of fibrosis in the heart and the propagation of fibrosis to other organs.

Aims and Approach

1.     Investigate the role of CD248 in BM remodeling and hematopoiesis post-MI. We will characterize the impact of the loss of CD248 on BM remodeling and hematopoiesis post-MI. We will use a pre-clinical model of MI and hematopoiesis assays.

2.     Determine the importance of CD248 in propagating fibrosis to distant organs post-MI. We will quantity fibrosis in multiple organs post-MI to determine the importance of CD248 in driving systemic fibrosis, using histological sections and advanced imaging quantification tools.

3.     Explore the mechanisms involved in BM remodeling and fibrosis in the heart. We will perform single nuclear RNA-seq analysis on the BM niche and the heart to get insight into the mechanisms driving BM remodeling and the perpetuation of fibrosis in the heart post-MI and how this may be impacted by the absence of CD248.

Training

The student will join an interdisciplinary research team and will be trained in all required biomedical techniques, including flow cytometry, hematopoiesis assays, echocardiography analysis, immunohistochemistry, imaging. The student will also be trained in R, single nuclear RNA-seq analysis, QuPath and Adobe Illustrator.

Contact details

For more information, please contact Dr Mihaela Crisan

Recruitment

This project will be suited to students with a strong interest in regenerative medicine, hematopoiesis and cardiovascular biology. Applicants must be of outstanding academic merit and research potential. Applicants should have obtained (or will soon obtain) a first or upper second-class UK honours degree or equivalent non-UK qualification, in a relevant subject area including biomedical sciences, immunology or biology. Research experience in flow cytometry, in vivo animal models, cell culture and/or imaging is desirable.

Application deadline

Friday 16th January 2026 (12noon, UK time)

Funding Notes

The successful candidate will receive a 3-year, fully-funded ‘Elizabeth Shields PhD Studentship’. This studentship is open to candidates who are eligible for tuition fees at UK Home Fee rate. The studentship offers a stipend (rate commensurate with the UKRI), and funds for research and travel.

The Studentship is named after Elizabeth Shields (née Kinross) who graduated in Zoology in 1966 from The University of Edinburgh. Elizabeth was Chair of the Mary Kinross Charitable Trust for many years, during which time the Trust funded projects in a range of topics, including biomedical research and renewable energy.

References

1. Travers et al., Circulation Research 2016
2. Benjamin et al., Circulation, 2019
3. Harjola et al., European Journal of Heart Failure 2017
4. Teicher BA. Oncotarget. 2019
5. Sa da Bandeira et al, 2017
6. Marvasti et al., J Am Heart Assoc. 2023

VIDA DTC - Investigation of vascular-oligodendrocyte interactions using iPSC-derived models of inherited vascular dementia

Closed for Applications

Supervisors: Dr Rikesh Rajani, Dr Tao Wang (University of Manchester), Prof Anna Williams
Centre/Institute: Institute for Regeneration and Repair

About the Project

About the Project

VIDA (Vascular and Immune contributors to DementiA) is a multi-institutional partnership between Alzheimer’s Society and four world-leading research sites: the University of Manchester, University of Edinburgh, Imperial, and City St George’s University of London. With projects focusing on the importance of vascular and immune mechanisms in dementia, VIDA PhD students will become the next generation of much-needed dementia researchers, contributing to breakthroughs in dementia diagnosis and treatment.

PhD studentships

VIDA students will embark upon a 4-year fully-funded PhD project at one of the four institutions above, with access to the state-of-the-art research facilities and interdisciplinary training available at all sites. Students at each site will come together as a cohort at several points during the programme, including annual conferences and residential workshop retreats which will link in with other Alzheimer’s Society Doctoral Training Centres across the UK. Students will also participate in engagement schemes with the Alzheimer’s Society and beyond, sharing the impact of their research in the community. The programme also benefits from built in opportunities for placements with leading industrial partners, and bespoke training plans including schemes to develop teaching, mentoring, and grant writing skills. 

Supervisors and Environment

Based at University of Edinburgh, Institute for Neuroscience and Cardiovascular Research, UK Dementia Research Institute 

Dr Rikesh Rajani (University of Edinburgh)

Prof Tao Wang (University of Manchester)

Prof Anna Williams (University of Edinburgh)

Project Background

Cerebral small vessel disease (SVD) is the leading cause of vascular dementia, and is characterised by white matter damage which correlates closely with the degree of cognitive impairment. SVD can be sporadic or inherited, and the most common inherited form of the disease is cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), which is caused by a mutation in the NOTCH3 gene. While we have previously shown some of the ways in which vascular changes can affect white matter in both sporadic and inherited SVD, we still don’t fully understand how these changes occur. Additionally, much of this previous work has relied on rodent models of disease, which do not fully recapitulate changes seen in human patients. 

In this project, the student will use human induced pluripotent stem cell (iPSC) derived cells to investigate interactions between vascular cells and oligodendrocytes (myelin forming cells in the brain) to better understand white matter damage in vascular dementia. We hypothesise that vascular cells derived from CADASIL patient iPSCs secrete factors which alter oligodendrocyte behaviour and function, including downstream effects of oligodendrocytes on neuronal activity and microglia. By identifying the molecules involved in these interactions, we hope to ultimately be able to disrupt these pathways to prevent disease pathology. 

The aims of the project are to: 

  • Develop a greater understanding of vascular and endothelial dysfunction in CADASIL, including changes in secreted molecules
  • Elucidate the mechanisms underlying oligodendrocyte changes in CADASIL
  • Identify secreted and other factors involved in mediating vascular induced oligodendrocyte changes in CADASIL, providing possible therapeutic targets to prevent white matter damage
  • Elucidate the role of oligodendrocytes in mediating neuronal and immune cell changes in CADASIL 

All of these aims will have high translational relevance through use of human patient-derived cells and human post-mortem tissue 

The student will be trained in iPSC cultures; differentiation of endothelial cels, mural cells, oligodendrocytes, neurons and microglia from iPSCs; functional characterisation of oligodendrocytes, neurons and microglia (including immunocytochemistry, live cell imaging and image analysis); histology, immunohistochemistry and in situ hybridisation on human post-mortem tissue; and molecular biology techniques (including ELISAs and proteomics). The student will be based primarily in Dr Rajani’s group at the University of Edinburgh, with short amounts of time spent in Prof Wang’s group at the University of Manchester to train in iPSC-mural cell differentiation. 

 

References

Rajani et al., Sci Trans Med 2018. DOI: 10.1126/scitranslmed.aam9507
Rajani et al., Acta Neuropathol Commun 2019. DOI: 10.1186/s40478-019-0844-x
Kelleher et al., Stem Cell Rep 2019. DOI: 10.1016/j.stemcr.2019.10.004
Rajani et al., Neuropathol Appl Neurobiol 2021. DOI: 10.1111/nan.12697

Funding Notes

Successful applicants will receive a generous stipend of £21,800 rising by £1,000 each year, and home fees will covered*. Funding is also provided for research expenses, career development and student travel/conference attendance.

*international student fees are covered by the University of Edinburgh for non-UK students if successful.

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MSc By Research: Regenerative Medicine and Tissue Repair Programme

Our MSc by Research in Regenerative Medicine and Tissue Repair is a one-year, full-time, on-campus Masters programme structured around two laboratory-based research projects and a research proposal writing component.

The programme is based at the Institute for Regeneration and Repair (IRR), a purpose-built research environment at the heart of Edinburgh BioQuarter, with a track record in training over 180 postgraduate students.

This MSc by Research is designed to prepare you for a research career in academia or industry, whether you have recently completed an undergraduate degree or are a professional who wants to pursue a career in research. You will gain valuable transferable skills that will be beneficial in a wide range of professions.

MSc By Research: Regenerative Medicine and Tissue Repair website

PhD Opportunities

PhD Students

If you are looking to join CRM as a PhD student, keep an eye on the FindaPhD website, where all studentships will be advertised.

Search for studendships on FindaPhD.com

Postdoctoral Research

To find a postdoc position, refer to the University of Edinburgh job search page,  where any postdoc/PDRA posts will be advertised. 

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Self Funded Applicants

We encourage inquiries and applications from self-funded basic and clinical scientists and from candidates who intend to apply for external funding all year round.

Instructions on how to apply as a self funded student

Studentships can include:

  • Stipend for 3 or 4 years
  • Tuition Fees
  • Research Training Costs
  • Conference Travel Allowance

Please contact relevant principal investigators informally to discuss potential projects and visit our funding opportunities page.

Information and contacts for principal investigators

PhD funding and finance

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