Professor Gerard Nash

Professor Gerard Nash

Institute of Cardiovascular Sciences
Director of Institute of Cardiovascular Sciences
Professor of Cardiovascular Rheology

Contact details

Institute of Cardiovascular Sciences
College of Medical and Dental Sciences
University of Birmingham
B15 2TT

Gerard Nash originally trained as a physical scientist and is interested in understanding the processes of cell adhesion and migration, and the effects of blood flow on these processes, by application of well-defined, quantitative, in vitro models.

Gerard has published over 200 research papers in scientific journals as well as reviews and book chapters in the fields of blood flow, cell mechanics, and leukocyte adhesion and migration. He has received grants from British Heart Foundation, Wellcome Trust, BBSRC, MRC, EPSRC and Cancer Research UK.


  • Ph.D. Biophysics, University of London, 1979
  • B.Sc. Physics (1st Class Honours), University of Manchester, 1975


After studying engineering and physics as an undergraduate, I opted to follow a research career in the biophysical sciences. My PhD was initially in instrumentation for automated cell characterisation but I quickly moved into cell mechanics and biorheology, and have subsequently gravitated towards studies of the cellular physiology of the cardiovascular system.

As a post-doc, my work at Guy’s and at University of Southern California  initially revolved around analysis of the physical properties of red cells, and later leukocytes, that influence their circulation. On returing to UK and St. George’s Hospital Medical School, I applied these analytical approaches to defining biomechanical abnormalities associated with vascular disease. 

On moving to Birmingham in 1989, my interest increasingly turned to the cellular adhesive properties of leukocytes and red cells. I established the Cardiovascular Rheology group, and developed novel flow-based culture and adhesion assays incorporating endothelial cells. We characterised for the first time the dynamic adhesive interactions of flowing malarial parasitised red cells. However, work on the mechanisms by which flowing neutrophils bind to ‘vessel’ walls came to take precedence, and we were the first to describe the ability of surface-adherent platelets to capture flowing neutrophils.   

At the same time I developed an increasing interest in the role of endothelial cells in regulating neutrophil recruitment. Studies followed, e.g, defining the ability of endothelial cells exposed to hypoxia, cigarette smoke or cytokines to induce neurophil recruitment, and defining the kinetics and molecular mechanisms of each stage of the capture, activation and migration process. More recently I have concentrated on the concept that the local physicochemical environment defines the responsiveness of endothelial cells to inflammatory stimuli, and also the subsequent fate of recruited leukocytes. This has involved development of models in which endothelial cells are conditioned by culture under different flow conditions or with different stromal cells. Initially we defined how these variables modified ability to capture and induce migration of leukocytes. We are currently extending this to include studies of migration through basement membrane into tissue constructs, and evaluation of how stromal cells may influence the fate of recruited leukocytes in inflammed tissue.

Much of the more recent work has been carried out in collaboration with Professors Ed Rainger, Chris Buckley and Steve Watson and Dr. Helen McGettrick, studying processes linked to development of chronic inflammatory pathology (such as atherosclerosis and rheummatoid arthritis) and to thrombo-inflammatory disorders.  We have worked on linking inflammatory responses with thrombosis and angiogenesis, and examining the potential for stem cells to modulate such responses. In this way we aim to develop an understanding of how these different responses are integrated and may be manipulated to facilitate tissue healing. This work is inter-disciplinary in nature, and e.g., acts as an interface between the Institute of Cardiovascular Sciences and the Institute of Inflammation and Ageing.


  • Lectures and small group teaching for cardiovascular and respiratory science to MBChB, BDS and Biomedical Sciences
  • Lectures for haematology for Biomedical Materials Science
  • Lectures in BMedSc Yr 3 options on Vascular Biology and Pathology, and Immunity and Inflammatory Disease
  • Supervises laboratory projects for Yr 3 BMedSc
  • Tutorials on cell recruitment from the circulation for MRes taught modules
  • Personal mentor for MBChB

Postgraduate supervision

Gerard is on the steering committee of the EPSRC Doctoral Research Centre ‘Physical Sciences for Health'.

He is interested in supervising doctoral research students in the following areas:

  • Mechanisms of leukocyte recruitment from the blood and migration into the vessel wall, and the effects of the local haemodynamic and stromal micro-environments on these processes
  • The role of disrupted leukocyte recruitment in vascular inflammatory disease
  • Mechanisms by which stem cells move from the vascular compartment into tissue and subsequently modulate leukocyte recruitment.

If you are interesting in studying any of these subject areas please contact Gerard on the contact details above.For a full list of available Doctoral Research opportunities, please visit our Doctoral Research programme listings.


Research Themes

  • Cardiovascular science and endothelial cell biology
  • Leukocyte adhesion and migration
  • Stem cell recruitment
  • Vascular pathology linked to abnormal leukocyte recruitment.

Cardiovascular rheology seeks to understand the physiological regulation of leukocyte adhesion and migration through endothelium, and to define how disruption of these processes occurs in vascular inflammatory diseases. There is emphasis on realistic in vitro modelling of leukocyte-endothelial interaction, using flow-based models which mimic the circulation, and on the physical environmental factors that influence leukocyte recruitment. Linked studies relate to modulation of endothelial sensitivity by the stromal environment, and atheroma formation (with Profs. Ed Rainger and Chris Buckley and Dr. Helen McGettrick). We are also interested in links between inflammation, thrombosis and angiogenesis as integrated responses to tissue injury.   Recently, we have incorporated studies of the recruitment of stem cells across endothelium, and of the ability of stem cells to modulate leukocyte recruitment. Collaborations exist with colleagues investigating inflammatory processes in rheumatoid arthritis, liver disease, traumatic injury, burns and post-surgical complications.

Other activities

  • Project Grants Committee, British Heart Foundation (2008 - 2012 )
  • External Examiner, Dept. Bioengineering, Imperial College (2009 - 2012 )
  • Editorial Board, Clinical Haemorheology and Microcirculation (1991 - )
  • Editorial Board, Biorheology (2001 - )
  • Co-Editor-in Chief, Biorheology (2013 - )
  • Co-Chair, International Society on Haemostais and Thrombosis, Scientific Standards Committee, Scientific Subcommittee on Biorheology (2001-2010)
  • Research Grants Committee, Queen Elizabeth Hospital Birmingham Charity
  • President, International Society for Clinical Hemorheology (2012-2015)


For a full list of publications go to:

Appleby SL, Mitrofan CG, Crosby A, Hoenderdos K, Lodge K, Upton PD, Yates CM,  Nash GB, Chilvers ER, Morrell NW. Bone Morphogenetic Protein 9 Enhances Lipopolysaccharide-Induced Leukocyte Recruitment to the Vascular Endothelium. J Immunol. 2016; 197:3302-3314

Munir H, Ward LSC, Sheriff L, Kemble S, Barone F, Nash GB, McGettrick HM. Adipogenic differentiation of MSC alters their immunomodulatory properties in a tissue-specific manner. Stem Cells 2017;  in press

Chimen M, McGettrick HM, Apta B, Kuravi SJ, Yates CM, Kennedy A, Odedra A, Alassiri M, Harrison M, Martin A, Barone F, Nayar S, Hitchcock JR, Cunningham AF, Raza K, Filer A, Copland DA, Dick AD, Robinson J, Kalia N, Walker LS, Buckley CD, Nash GB, Narendran P, Rainger GE. Homeostatic regulation of T cell trafficking by a B cell-derived peptide is impaired in autoimmune and chronic inflammatory disease. Nat Med. 2015;21:467-75.

Luo D, McGettrick HM, Stone PC, Rainger GE, Nash GB. The roles of integrins in function of human neutrophils after their migration through endothelium into interstitial matrix. PLoS One. 2015; 10:e0118593.

Luu NT, McGettrick HM, Buckley CD, Newsome PN, Rainger GE, Frampton J, Nash GB. Crosstalk between mesenchymal stem cells and endothelial cells leads to downregulation of cytokine-induced leukocyte recruitment. Stem Cells. 2013; 3: 2690-702

Watts T, Barigou M, Nash GB. Comparative rheology of the adhesion of platelets and leukocytes from flowing blood: why are platelets so small? Am J Physiol Heart Circ Physiol. 2013;304:H1483-94

Glen K, Luu NT, Ross E, Buckley CD, Rainger GE, Egginton S and Nash GB (2012) Modulation of functional responses of endothelial cells linked to angiogenesis and inflammation by shear stress: differential effects of the mechanotransducer CD31J Cell Physiol 227(6):2710-21

Burton VJ, Butler LM, McGettrick HM, Stone PC, Jeffery HC, Savage CO, Rainger GE and Nash GB (2011) Delay of migrating leukocytes by the basement membrane deposited by endothelial cells in long-term cultureExp Cell Res 317(3):276-92

Butler LM, Jeffery HC, Wheat RL, Rae PC, Townsend K, Alkharsah KR, Schulz TF, Nash GB, Blackbourn DJ (2011) Kaposi's sarcoma-associated herpesvirus infection of endothelial cells inhibits neutrophil recruitment through an interleukin-6-dependent mechanism: a new paradigm for viral immune evasion. J Virol 85(14):7321-32


Cardiovascular Rheology