Christina Warboys

Christina Warboys

Dr

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Biographical details

Christina studied Medical Biochemistry (BSc Hons) at the University of Leicester before completing a PhD in Cardiovascular Physiology at King’s College London. During her doctoral studies Christina investigated the acute effects of glycated proteins on the permeability of the retinal microvasculature, with a view to understanding the early signalling mechanisms occurring in diabetic retinopathy.

In 2006, Christina began her postdoctoral research in the Department of Bioengineering at Imperial College London under the guidance of Professor Peter Weinberg investigating transendothelial mass transport in vitro and the effects of shear stress on endothelial cell permeability.  A proposed initiating event in the development of atherosclerosis is the excessive entry of macromolecules into the vessel wall which has been associated with low wall shear stress and flow reversal during the cardiac cycle. A link between these two was provided during this study where chronic exposure to unidirectional shear stress was found to reduce endothelial permeability. Christina also studied the role of vascular dendritic cells (VDCs) in modulating endothelial permeability. VDCs are found in the intimal layer of large arteries and it was hypothesised they may be able to modulate vascular function, as supporting cell types e.g. astrocytes do in the cerebral vasculature. Christina found that co-culture of endothelial cells with VDCs reduced permeability although the mechanism remains to be determined and is now the focus of ongoing research. During her time in Bioengineering, Christina also taught on the Medical Sciences module of the Undergraduate Bioengineering Degree and took an active role in lab management and safety.

In 2010 Christina moved to the National Heart and Lung Institute at Imperial College to work for Dr. Paul Evans on a multi-disciplinary British Heart Foundation-funded project looking at the effects of flow and shear stress on endothelial apoptosis and senescence.  These studies aimed to improve our understanding of the focal distribution of atherosclerosis. One of the key findings was that endothelial senescence (associated with vascular aging) was accelerated by disturbed flow in vitro and that senescent cells accumulate in vivo at sites of low/disturbed flow before the onset of atherosclerotic lesions – potentially indicating a role in causing or accelerating cardiovascular disease.  Christina also found that activation of Sirt1 (associated with longevity and survival) could reduce this effect and that cells exposed to uniform flow (and protected from atherosclerosis), had higher expression of this enzyme. Parallel studies of arterial endothelial cells exposed to low/disturbed low compared to undisturbed flow also revealed differential regualtion of the apoptotic programme. Studies are ongoing to determine the functional significance. During her time within the NHLI, Christina was also a member of the NHLI postdoctoral committee. 

In October 2012 Christina moved back to the Cardiovascular Division at King's College London to take up a research post with Professor Albert Ferro funded by the British Heart Foundation. Christina is studying the interaction between two key regulators of endothelial function, nitric oxide and β-catenin.  The project aims to determine how alterations in these interations may contribute to endothelial dysfunction, a key initiating factor in the development of atherosclerosis.

Expertise related to UN Sustainable Development Goals

In 2015, UN member states agreed to 17 global Sustainable Development Goals (SDGs) to end poverty, protect the planet and ensure prosperity for all. This person’s work contributes towards the following SDG(s):

  • SDG 3 - Good Health and Well-being

Education/Academic qualification

Doctor of Philosophy, Mechanisms by which RAGE activation acutely increases retinal microvascular permeability, King's College London

Award Date: 1 Jan 2006

Bachelor of Science, University of Leicester

Award Date: 1 Jan 2002

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