Research groupsWe currently have one funded studentships available
Deadline May 28th 2017.
David Bates and Alan McIntyre, in conjunction with MRC Harwell (Lydia Teboul) and Exonate Ltd
For more information and to apply, go to: http://www.birmingham.ac.uk/schools/mds-graduate-school/scholarships/mrc-impact/apply.aspx
This is an MRC funded studentship
to start in October 2017 funded through the MRC
Integrated Midlands Partnership for Biomedical Training.
(IMPACT). It is based in Nottingham, but a few weeks
will be spent at the MRC Harwell Transgenic unit in
Oxfordshire. It comes with a 3.5 year stipend, full fees
paid for for home/EU students, and a cohort training
program that is joint between the Universities of
Birmingham, Leicester and Nottingham. Applicants must
have a first or a 2:1 - a Masters degree often helps but
is not required. Feel free to call Prof Bates to discuss
this on 0115 823 1135.
Diabetics have increased risk of cardiovascular disease. In non-diabetic patients, when blood vessels block, the body generates new vessels circumventing the blockage, but this collateral growth is less common in diabetics. Blood vessel growth, (angiogenesis), occurs in response to vascular endothelial growth factor (VEGF), generated in white blood cells that home to tissue with poor blood supply. VEGF can be made in multiple types, some of which stimulate angiogenesis and others that prevent it. Using mouse models, we discovered that one of the reasons why collaterals do not form as well in diabetes is that the type of VEGF made in diabetic patients is anti-angiogenic. We also confirmed that in humans, this anti-angiogenic VEGF is found more in diabetic than non-diabetic patients. Anti-angiogenic VEGF expression is stimulated by a circulating protein called Wnt5a. This project will find out whether human diabetics have the same control of collateral formation by Wnt5a, and how Wnt5a causes the cells to make the anti-angiogenic form of VEGF. If we can pinpoint this mechanism then we will try and change the production of VEGF so that blood vessels can grow again in diabetic mice. This could lead to new treatments for cardiovascular disease in diabetics. The project will benefit from a close association with Exonate Ltd, a pharmaceutical company developing compounds that can change VEGF expression in vivo, and that will provide training in an industrial context in a growing drug discovery company.
Some references from host lab:
- Kikuchi et al An anti-angiogenic isoform of VEGF-A contributes to impaired vascularization in peripheral artery disease Nature Medicine 2014. 20(12):1464-71 X Ye et al.
- Anti-angiogenic VEGF-A variants, one of the factors underlying infantile hemangioma involution. J Pathology. 2016 239(2):139-51
- OA Stone, et al. Differential regulation of blood flow induced neovascularisation and mural cell recruitment by VEGF and angiopoietin signalling. J Physiol in press