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Dr Tim Chico

Tim Chico graduated from Leeds Medical School in 1993. After General Medicine training he undertook an MD with Prof David Crossman at the University of Sheffield. After postdoctoral research at Genentech Inc, he became Clinical Lecturer in Cardiology in Sheffield. In 2004 was awarded a GSK Clinician Scientist Fellowship to develop the zebrafish as a novel model of arteriogenesis. Since 2006 he has been Senior Clinical Lecturer and honorary Consultant Cardiologist and works within the MRC Centre for Developmental and Biomedical Genetics and the NIHR Cardiovascular Biomedical Research Unit in Sheffield.

Research

Summary for nonspecialist

After an arterial blockage, "collateral vessels" can develop by a process called arteriogenesis which improves blood supply. Studying arteriogenesis using mammals is difficult because a) visualising arteries is technically challenging, b) it is time-consuming to remove single genes to study their effect, and c) when an artery is blocked, lack of oxygen (hypoxia) induces processes unrelated to arteriogenesis. In my group we discover genes involved in arteriogenesis using zebrafish embryos, because a) their transparency makes visualisation of vessels easy, b) we can quickly and easily reduce their gene expression and c) they does not suffer hypoxia after arterial blockage, since oxygen diffuses from the water. Increasing our understanding of arteriogenesis may ultimately generate novel therapies for patients with with occluded arteries.

Technical Summary

Arteriogenesis (collateral vessel formation) has the potential to ameliorate the consequences of arterial occlusion. However, only a third of patients develop collateral vessels and may factors such as age and diabetes impair arteriogenesis. Very little is known about the genetic and cellular regulation of arteriogenesis, in part due to the technical challenges of studying this in mammals. We therefore use zebrafish that are genetically tractable and allow excellent visualisation of the vasculature. We are able to study the response to arterial occlusion and knockdown specific genes by morpholino antisense to determine their contribution to arteriogenesis.

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