The symposium is organised by DRA and DSMB and is free of charge and open for attendance by all interested parties. It is not necessary to pre-register.
Program
| 12:45 | Auditorium open and possibility to grab a coffee |
| 13:00 | Introduction
Assoc. Prof. Andrea Heinz, Department of Pharmacy, University of Copenhagen, Denmark |
| 13:05 | Detecting and repairing damage in tissue extracellular matrices
Prof. Michael Sherratt, School of Biological Sciences, University of Manchester, UK |
| 14:00 | Extracellular matrix and other protein changes in human cardiovascular disease
Prof. Michael Davies, Biomedical Institute, University of Copenhagen, Denmark |
| 15:00 | Closing of the DRA symposium |
This DRA symposium provides DRA PhD students with the opportunity to engage with cutting-edge research on extracellular matrix (ECM) damage and its implications in age-related pathologies such as skin aging or atherosclerosis. By focusing on advanced techniques such as phase contrast micro-computed tomography 3D imaging, mass spectrometry and peptide location fingerprinting, PhD students will gain insights into innovative methods for analyzing ECM structure and function. This symposium also exposes students to interdisciplinary approaches, from in silico predictions to in vivo testing, fostering a comprehensive understanding of ECM-related diseases and potential therapeutic strategies. Through these interactions, PhD students will be able to better appreciate the translational potential of their research and enhance their skills in both basic and applied science around the ECM and protein analysis.
The symposium is organized on behalf of the graduate programme in pharmaceutical sciences, Drug Research Academy, by Associate Professor Andrea Heinz, Department of Pharmacy, Faculty of Health and Medical Sciences, University of Copenhagen and the Danish Society for Matrix Biology
Talk 1: Detecting and repairing damage in tissue extracellular matrices
Prof. Michael Sherratt, School of Biological Sciences, University of Manchester, UK, michael.j.sherratt@manchester.ac.uk
Abstract:
Damage to extracellular matrices is a key factor in many age-related pathologies. This damage may manifest as changes in both whole tissue architecture and the structure of component proteins. We have developed phase contrast microCT 3D imaging approaches which can detect and quantify age- and disease-related re-modelling in elastic arteries, and which can map 3D mechanical properties in the intervertebral disc. We have also developed a novel mass spectrometry analysis approach: peptide location fingerprinting (PLF), which can identify structurally compromised ECM proteins, many of which exhibit similar damage molecular damage profiles across organs, species and due to exposure to radiotherapeutic X-ray doses.
This PLF approach has also been used to identify ECM targets of chronic photo-ageing in human skin. In order to repair this photo-damage, we tested the hypothesis that small peptides may act as matrikines inducing repair by resident skin cells. Recently, we described an in silico to in vitro to in vivo discovery to predict, synthesize, screen and characterize peptide matrikines. The predicted matrikines exhibited sequence-specific modulation of cultured human dermal fibroblast proteomes in vitro and, when applied to skin, enhanced the transcription of genes that promoted epithelial and dermal remodelling in human volunteers. In ongoing studies we are exploring their mechanisms of action against multiple cell types.
Short bio:
Michael Sherratt is an academic Professor in the division of Cell Matrix Biology & Regenerative Medicine at the University of Manchester. His research is focused on characterising the causative mechanisms and the structural and mechanical consequences of ageing in extracellular matrix rich tissues including skin, arteries, breast and cartilage. In order to achieve these goals, his lab has: i) developed novel atomic force microscopy and microCT methodologies to visualise tissue architecture and in health and disease, ii) demonstrated that elastic fibre associated proteins are key targets of ultraviolet radiation, X-rays and oxidation and iii) shown that bioinformatic and mass spectrometry approaches can be used to identify novel ageing biomarkers and fingerprints of damage. Recently, in collaboration with Boots/No 7 Beauty Company, he has directed a project to predict and characterise the ability of novel extracellular matrix peptides to enhance the expression of genes which support skin function and promote natural self-repair. Graduate programme in pharmaceutical sciences, Drug Research Academy, DRA
Talk 2: Extracellular matrix and other protein changes in human cardiovascular disease
Prof. Michael Davies , Department of Biomedical Sciences, University of Copenhagen, Denmark, davies@sund.ku.dk
Abstract:
The extracellular matrix (ECM) plays a key role in determining the architecture of tissues and the behavior of cells. Considerable data support the hypothesis that changes to the ECM plays a key role in determining whether atherosclerotic plaques present in human arteries are stable and non-life threatening, or are unstable and undergo rupture resulting in a heart attack or stroke. This presentation will discuss the role of various proteomic (and other) methods in examining these plaque differences, the underlying mechanisms of matrix dam-age and potential therapeutic avenues.
Short bio:
Michael Davies received his BSc and DPhil degrees from the University of York, UK. After post-doc work in London, he worked as a Lecturer at the University of York, before moving to Australia, to take up a position at the Heart Research Institute in Sydney. 17 years later, after serving as both Deputy-Director and Director of the Heart Research Institute, he moved to the University of Copenhagen to take up a Novo Nordisk Foundation Laureate grant. His research work is focused on understanding the mechanisms and significance of protein alterations, including post-translational modifications and redox changes, in human disease, with a particular emphasis on atherosclerosis.
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