John Greenwood
Short biography:
Professor John Greenwood holds the Hugh Davson Chair of Biomedical Research and is Head of the Department of Cell Biology at the UCL Institute of Ophthalmology, University College London. He obtained his PhD from the Institute of Psychiatry, University of London following a study of nutrient transport systems of the specialised blood vessels of the brain and how this structure, termed the blood-brain barrier (BBB), contributed to brain disease. This work led to the identification and characterisation of a transport system at the BBB for thiamine (vitamin B1). After a two-year postdoctoral fellowship in the Blood-Brain Barrier Group at King’s College London, he was awarded in 1990 the Renee Hock Fellowship at the UCL Institute of Ophthalmology to study the role of the blood-retinal barrier (BRB) in retinal inflammatory disease. In 1993 he was made Senior Lecturer at the Institute of Ophthalmology and in 2000 he was appointed Full Professor.
The Greenwood laboratory focuses on the roles of retinal and brain vascular endothelial cells and retinal pigment epithelial (RPE) cells in the context of disease. His research staff occupies state-of-the-art laboratories in the Henry Wellcome Building for Translational Eye Research at the UCL Institute of Ophthalmology. This new building was the result a successful £9.2M application led by Greenwood and was funded by the Wellcome Trust and Fight for Sight (UK). Since 2004 he has developed a strong and fruitful collaboration with Professor Stephen Moss at the Institute of Ophthalmology.
Vascular Research
Research into the role the vascular endothelium in the pathogenesis of retinal and brain inflammation is a major component of the laboratory. A significant part of this research addresses the role the vascular endothelium plays in diseases such as posterior uveitis and multiple sclerosis (MS). Such work has been at the forefront of identifying and characterising novel endothelial cell mechanisms that facilitate the recruitment of leukocytes to the retina and brain, a critical step in the pathogenesis of neuroinflammatory diseases. This work established the principle of outside-in signalling in CNS endothelial cells mediated through leukocyte engagement of endothelial cell adhesion molecules and the downstream effector mechanisms that support leucocyte transvascular migration. With this information the Greenwood lab has been able to design novel therapeutic approaches to target these critical pathways in order to reduce leukocyte recruitment and attenuation the disease process. This work has led to a successful clinical trial of statins in secondary progressive MS.
More recently, vascular biology research in the Greenwood laboratory has focussed on the biology underpinning vascular complications in diseases such as macular telangiectasia, diabetic retinopathy and neovascular (wet/neovascular) age-related macular degeneration (AMD). This work has resulted in the identification and characterisation of a novel pro-angiogenic factor called leucine-rich alpha-2-glycoprotein 1 (LRG1) and has led to the development of a therapy targeting this protein. A UK Medical Research Council grant was awarded to take this work forward into a phase I/IIa clinical trial in wet AMD. A company, Senya Therapeutics (https://senyatx.com) has been spun out from UCL to commercialise therapies targeting LRG1. Greenwood is a founding scientist and a senior scientific advisor to SenyaTx.
Retinal Pigment Epithelial Cell Research
Understanding the role of RPE cells in the development of retinal diseases, such as age-related macular degeneration (AMD), constitutes an additional focus of the Greenwood laboratory. Developing immortalised RPE cell-based therapies for AMD established the principle of using immortalised cells for treatment of AMD. The laboratory has also been engaged in research to investigate the role of RPE in AMD and gain insight into the cellular mechanisms underpinning this disease. This has resulted in key publications defining the role of complement factor H and the RPE in retinal dysfunction.
Address: Department of Cell Biology
UCL Institute of Ophthalmology
11-43 Bath Street
London EC1V 9EL
United Kingdom
Professor John Greenwood holds the Hugh Davson Chair of Biomedical Research and is Head of the Department of Cell Biology at the UCL Institute of Ophthalmology, University College London. He obtained his PhD from the Institute of Psychiatry, University of London following a study of nutrient transport systems of the specialised blood vessels of the brain and how this structure, termed the blood-brain barrier (BBB), contributed to brain disease. This work led to the identification and characterisation of a transport system at the BBB for thiamine (vitamin B1). After a two-year postdoctoral fellowship in the Blood-Brain Barrier Group at King’s College London, he was awarded in 1990 the Renee Hock Fellowship at the UCL Institute of Ophthalmology to study the role of the blood-retinal barrier (BRB) in retinal inflammatory disease. In 1993 he was made Senior Lecturer at the Institute of Ophthalmology and in 2000 he was appointed Full Professor.
The Greenwood laboratory focuses on the roles of retinal and brain vascular endothelial cells and retinal pigment epithelial (RPE) cells in the context of disease. His research staff occupies state-of-the-art laboratories in the Henry Wellcome Building for Translational Eye Research at the UCL Institute of Ophthalmology. This new building was the result a successful £9.2M application led by Greenwood and was funded by the Wellcome Trust and Fight for Sight (UK). Since 2004 he has developed a strong and fruitful collaboration with Professor Stephen Moss at the Institute of Ophthalmology.
Vascular Research
Research into the role the vascular endothelium in the pathogenesis of retinal and brain inflammation is a major component of the laboratory. A significant part of this research addresses the role the vascular endothelium plays in diseases such as posterior uveitis and multiple sclerosis (MS). Such work has been at the forefront of identifying and characterising novel endothelial cell mechanisms that facilitate the recruitment of leukocytes to the retina and brain, a critical step in the pathogenesis of neuroinflammatory diseases. This work established the principle of outside-in signalling in CNS endothelial cells mediated through leukocyte engagement of endothelial cell adhesion molecules and the downstream effector mechanisms that support leucocyte transvascular migration. With this information the Greenwood lab has been able to design novel therapeutic approaches to target these critical pathways in order to reduce leukocyte recruitment and attenuation the disease process. This work has led to a successful clinical trial of statins in secondary progressive MS.
More recently, vascular biology research in the Greenwood laboratory has focussed on the biology underpinning vascular complications in diseases such as macular telangiectasia, diabetic retinopathy and neovascular (wet/neovascular) age-related macular degeneration (AMD). This work has resulted in the identification and characterisation of a novel pro-angiogenic factor called leucine-rich alpha-2-glycoprotein 1 (LRG1) and has led to the development of a therapy targeting this protein. A UK Medical Research Council grant was awarded to take this work forward into a phase I/IIa clinical trial in wet AMD. A company, Senya Therapeutics (https://senyatx.com) has been spun out from UCL to commercialise therapies targeting LRG1. Greenwood is a founding scientist and a senior scientific advisor to SenyaTx.
Retinal Pigment Epithelial Cell Research
Understanding the role of RPE cells in the development of retinal diseases, such as age-related macular degeneration (AMD), constitutes an additional focus of the Greenwood laboratory. Developing immortalised RPE cell-based therapies for AMD established the principle of using immortalised cells for treatment of AMD. The laboratory has also been engaged in research to investigate the role of RPE in AMD and gain insight into the cellular mechanisms underpinning this disease. This has resulted in key publications defining the role of complement factor H and the RPE in retinal dysfunction.
Address: Department of Cell Biology
UCL Institute of Ophthalmology
11-43 Bath Street
London EC1V 9EL
United Kingdom
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