About the Project
We are studying the molecular mechanisms associated with the formation of abnormal arterio-venous connections in cAVM. In cAVM, the ‘angioarchitecture’ (i.e. the shape and size of these blood vessel abnormalities) can change, and in some cases new blood vessels develop in a process called angiogenesis. Experimental work has shown that a signalling protein called Vascular Endothelial Growth Factor (VEGF), which stimulates angiogenesis, is found at high levels in cAVM and represents a promising treatment target , however further investigation is necessary. Using zebrafish disease models [3-5], we aim to further characterise the development of cAVMs over time and investigate the role of defective angiogenic processing in this pathology. Furthermore, we will perform pharmacological intervention studies to determine whether manipulation of angiogenesis signalling pathways (e.g. VEGF inhibition) can limit cAVM formation. This work will improve our understanding of the role of VEGF in cAVM development and determine whether VEGF represents a realistic therapeutic target for this condition in the future.
Training/techniques to be provided:
Home Office personal licence.
Zebrafish disease modelling.
This project has a Band 3 fee. Details of our different fee bands can be found on our website (View Website). For information on how to apply for this project, please visit the Faculty of Biology, Medicine and Health Doctoral Academy website (View Website).
Informal enquiries may be made directly to the primary supervisor.
2. Mouchtouris, N., et al., Biology of cerebral arteriovenous malformations with a focus on inflammation. J Cereb Blood Flow Metab, 2015. 35(2): p. 167-75.
3. Rochon, E.R., P.G. Menon, and B.L. Roman, Alk1 controls arterial endothelial cell migration in lumenized vessels. Development, 2016. 143(14): p. 2593-602.
4. Roman, B.L., et al., Disruption of acvrl1 increases endothelial cell number in zebrafish cranial vessels. Development, 2002. 129(12): p. 3009-19.
5. Sugden, W.W., et al., Endoglin controls blood vessel diameter through endothelial cell shape changes in response to haemodynamic clues. Nature Cell Biology, 2017. 19(6): p. 653-665.
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