The Leeds Institute of Genetics, Health and Therapeutics (LIGHT) focuses on laboratory, clinical and applied biomedical research into common chronic disorders and non-communicable disease. This includes research into cardiovascular disease, diabetes, cancer, neurodegenerative diseases, reproduction and early development, child health and lifecourse epidemiology.
The institute has a strong focus in population health and applied health research, underpinned by expertise in biomedical imaging, biostatistics and epidemiology, including exposure assessment. Our research leads to both prevention strategies in populations and improved treatment and disease management. We aim to increase the impact of our research by protecting our intellectual property to enable translation of our research into development of novel therapies and medical devices to address unmet clinical needs. This is achieved via the co-ordination of activity between our Institute, Faculty and the University Commercialisation Services.
As an integral part of the School of Medicine delivering cutting edge research, LIGHT is committed to the transfer of knowledge to students at both undergraduate and postgraduate levels. LIGHT hosts postgraduate research students, runs postgraduate taught courses and makes significant contributions to undergraduate teaching, including the MBChB and intercalated BSc Clinical Science programmes in Medical Imaging and Cardiovascular Medicine.
Professor Mark S Gilthorpe
Professor Mark Kearney (Division of Cardiovascular) is fronting the British Heart Foundation’s latest campaign to raise awareness of heart disease and the work of academics and clinicians across the UK. Here he is interviewed by the Observer’s Science Editor Robin McKie.
Read more about Professor Kearney’s role in the campaign here.
Watch their television advert, which features Prof Kearney.
Karen Porter and colleagues, in collaboration with a collaborator in Canada, have just published a paper in the International Journal of Biochemistry and Cell Biology, entitled:
Apolipoprotein(a) acts as a chemorepellent to human vascular smooth muscle cells via integrin αVβ3 and RhoA/ROCK-mediated mechanisms.
Kirsten Riches, Larissa Franklin, Azhar Maqbool, Michelle Peckham, Matthew Adams, Jacquelyn Bond, Philip Warburton, Nicole T. Feric, Marlys L. Koschinsky, David J. O’Regan, Stephen G. Ball, Neil A. Turner, Karen E. Porter.
Read the full article.
A little bit about the background to the study:
It is well established that a key risk factor for cardiovascular disease is high circulating levels of LDL cholesterol. However increased levels of another plasma lipoprotein, lipoprotein(a) [Lp(a)], have also been identified as a highly heritable risk factor that unlike cholesterol cannot be controlled by diet or drug therapy.
As Lp(a) is only expressed in humans and some primates, studies are restricted to tissue from these sources and interpretation of data from animal models is challenging. The key functional component of Lp(a) is apo(a) which can be expressed and purified in vitro, and was provided by our Canadian collaborator for this study.
We studied the effect of apo(a) on human saphenous vein smooth muscle cells (SV-SMC) and discovered that apo(a) adversely modulates SMC function in a way that is likely to be detrimental to venous bypass graft patency.
Whilst a receptor for Lp(a) has not been discovered, we elucidated some of the mechanisms via which apo(a) causes aberrant SV-SMC function as step towards finding alternative therapeutic targets.