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Personal profile


Ray Boot-Handford is a Professor of Biochemistry within the Wellcome Trust Centre for Cell-Matrix Research. He is the Academic Lead for the Manchester BBSRC Doctoral Training Partnership.  Ray chaired the British Society for Matrix Biology (2009-2015) and has served on the Arthritis Research UK Research Grant Subcommittee (1996-2000 & 2011-2015).

Ray obtained a Biochemistry degree from University College, Cardiff (1976) and PhD from University College London (1980). Ray moved to a postdoc with Mike Grant in Manchester to research basement membrane changes in diabetes. In 1985 Ray was awarded a Lions Club Fellowship to continue his work firstly at Rutgers Medical School, NJ, USA and more latterly at newly formed Jefferson Institute of Molecular Medicine in Philadelphia. In 1987, he returned to The University of Manchester on a RNIB Fellowship and was appointed to a lectureship in 1989. Ray’s lab was the first to clone mammalian collagen X sequences and went on to identify chondrodysplasias associated with mutations in collagen X. In 1999, Ray was awarded a Wellcome Trust Research Leave Fellowship to learn and apply mouse gene targeting techniques. The major current focus of the lab is in determining disease mechanisms associated with osteoarthritis and with mutations in cartilage genes such as type X collagen using in vivo mouse models of disease.

Research interests

ER stress as a pathogenic factor in cartilage

Work in my lab is focused on answering two questions relating to the structure and function of cartilage in development and disease. Firstly: What is the role of ER stress in the pathogenesis of diseases mediated by chondrocytes such as chondrodysplasias and osteoarthritis?  We have shown an association of ER stress with disease pathology using cell culture and in-house generated knock-in mouse models of chondrodysplasia caused by mutations in cartilage ECM genes such as collagen X, COMP and matrilin 3. Furthermore, by generating novel transgenic lines in which elevated ER stress (caused by the expression of a non-secreted, ER stress-inducing protein) is targeted to relevant chondrocytes in vivo by use of the collagen X or II promoter, we have demonstrated the capability of ER stress to induce chondrodysplasia. Our current efforts are focused on genetically dissecting out the roles of different ER stress pathways in disease pathogenesis using a series of conditional ER stress-related mouse lines crossed with our own chondrodysplasia lines. We are also characterising the consequences of elevated ER stress in the pathogenesis of osteoarthritis using a mechanically-induced disease model.
Secondly, we are using cell culture and in vivo models to test: Does alleviating ER stress by various pharmacological interventions reduce disease severity? These approaches may lead to novel therapeutic opportunities for treating a variety of chondrodysplasias and osteoarthritis.


Most of the bones of our body develop and grow by way of a cartilage template in a process called endochondral ossification. Cartilage has a single cell type, known as the chondrocyte, which secretes the abundant extracellular matrix in which these cells are embedded. The cartilage template of the skeleton deposited during development is transformed to bone in a highly organised developmental sequence that drives bone growth. Mutations in the genes encoding the cartilage ECM affect the way in which our long bones grow and result in a range of diseases classed as chondrodysplasias, the major feature of which is dwarfism. Chondrodysplasias are also often associated with early-onset osteoarthritis where the articular cartilage degrades causing joint failure and significant pain. Our studies are focused on understanding how cartilage ECM proteins function, defining the mechanisms by which mutations in cartilage proteins cause chondrodysplasia, and understanding the mechanisms by which osteoarthritis develops. Defining precisely the mechanisms by which these diseases develop has the potential to highlight new opportunities for treatment which is the long-term goal of these studies.


Ray lectures on the final year undergraduate course entitled Biochemical Basis of Disease.  He also actively participates in delivering Medicine Problem Based Learning and is a final year academic tutor for Medical Biochemistry.

Expertise related to UN Sustainable Development Goals

In 2015, UN member states agreed to 17 global Sustainable Development Goals (SDGs) to end poverty, protect the planet and ensure prosperity for all. This person’s work contributes towards the following SDG(s):

  • SDG 3 - Good Health and Well-being

Research Beacons, Institutes and Platforms

  • Manchester Regenerative Medicine Network


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