Research themes
Departments and Institutes
- Department of Medicine:
- Postdoctoral Associate
- Cardiovascular Strategic Research Initiative:
Research Interests
Interleukin-1α signalling from endothelial cells and its involvement in the development of atherosclerosis and graft rejection
Abnormal thickenings in the arteries, known as atherosclerotic plaques, can cause significant cardiovascular problems. Cell types prevalent in plaques such as vascular smooth muscle cells, endothelial cells and macrophages undergo cell death and over time this cell death causes the plaque to become unstable. Plaque instability increases the chances of plaque rupture which can lead to heart attacks and stroke.
Previous work has demonstrated that IL-1α, a small protein released from dying cells, is responsible for inducing inflammatory responses in atherosclerotic plaques. This signalling pathway is well documented in vascular smooth muscle cells, but it is not known whether IL-1α released from endothelial cells produces the same inflammatory effects. This project will determine if endothelial derived IL-1α is capable of inducing inflammation and the mechanisms involved. Additionally, potential links between IL-1α derived inflammation and thrombosis will be examined with the intention of determining a novel relationship between thrombus formation and unstable atherosclerotic plaques.
Keywordsvascular smooth muscle cells (VSMC) ; endothelial function ; inflammation |
Topics
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Collaborators
Key Publications
Interleukin-1α Activity in Necrotic Endothelial Cells Is Controlled by Caspase-1 Cleavage of Interleukin-1 Receptor-2: IMPLICATIONS FOR ALLOGRAFT REJECTION. Burzynski LC, Humphry M, Bennett MR, Clarke MC. J Biol Chem. 2015 Oct 9;290(41):25188-96.