If you made any changes in Pure these will be visible here soon.

Personal profile

Current Research Interests

Myocardial infarction (MI) or heart attack most commonly occurs secondary to thrombus formation on a ruptured atherosclerotic plaque. The resulting loss of oxygen supply or ischaemia leads to death of tissue supplied by the blocked artery. Efficient intervention to remove thrombus and restore blood supply to the myocardium has improved short-term survival following MI, but the heart is frequently left with damage. Unlike some other organs the heart is not able to efficiently replace damaged myocardium through regeneration,  and instead replaces it by a scar that does not contribute to contraction. In the longer term the remaining healthy heart undergoes compensatory remodelling while trying to maintain cardiac output, leading to an increased chance of developing of debilitating chronic heart failure.

My research is focused primarily on understanding how to limit the loss of contractile tissue that occurs after MI, to prevent the stimulus for progression to heart failure. This includes tissue loss associated with acute ischaemia and the subsequent restoration of blood supply or reperfusion, but in particular the processes involved in infarct healing (neutrophils, macrophage polarisation, fibroblast activation & angiogenesis) and how these might be targeted therapeutically to prevent infarct expansion during repair. The mammalian myocardium retains regenerative capacity in the early post-natal period, my lab is studying the role of macrophages in growth and repair of the neonatal myocardium with a view to understanding how to enhance regenerative potential in the adult.

Current studies include investigation of intracellular glucocorticoid regeneration, interleukin-4 receptors, hydrogen sulphide metabolism and macrophage Wnt signallng.

Advanced in vivo imaging is key to identifying myocardial injury as well as in characterisation of structure, function and increasingly molecular processes during remodelling of the heart.  The lab collaborates extensively with Medical Physicists supporting the Edinburgh Preclinical Imaging unit to optimise the use of high frequency ultrasound, magnetic resonance imaging (MRI), positron emission tomography (PET) and optical imaging (fluorescence molecular tomography in vivo and optical projection tomography in vitro) for more accurate identification of viable myocardium post-MI, as well as structural and functional characterisation in health and disease.

My research in a nutshell

Survival following acute myocardial infarction (MI), or heart attack, has increased thanks to efficient intervention to restore blood supply to the myocardium, or heart muscle. However, the myocardium still incurs damage, and as the adult heart does cannot efficiently regenerate new tissue, a fibrous scar is formed that does not contribute to contraction. In the longer term the remaining healthy heart undergoes remodelling while trying to maintain cardiac output, leading to an increased chance of developing of debilitating chronic heart failureMy research is focused primarily on understanding how to limit the loss of contractile tissue that occurs immediately after MI, but in particular the processes involved in infarct healing (inflammation, fibroblast activation & angiogenesis) and how these might be targeted therapeutically to prevent infarct expansion during repair. We also work on development of new imaging techniques to identify vulnerable peri-infarct myocardium and on the mechanisms that support neonatal heart regeneration after injury.  

see Research in Nutshell video:  http://www.nutshell-videos.ed.ac.uk/gillian-gray-myocardial-injury-repai...

Biography

Gillian Gray obtained her B.Sc. with Honours in Pharmacology from the University of Aberdeen. Her Ph.D. studies at the University of Strathclyde with Brian Furman and James Parratt identified PAF and PGE2 as key mediators in sepsis induced hypotension and loss of vascular function. In 1988 Gillian took up a post-doctoral fellowship at the  Université Louis Pasteur de Strasbourg, France with Jean-Claude Stoclet to continue studies of vascaulr dysfunction in sepsis. This lead to  the first description of the role of inducible nitric oxide synthase (iNOS) in sepsis associated hypotension and vascular dysfunction (Gray et al.,1990. Br. J. Pharmacol. 103, 1218-1224). Gillian then joined the CV research group led by Martine Clozel at F. Hoffman-La Roche, Basel, Switzerland, studying receptors that mediated the effects of the newly described potent vasoconstrictor peptide, endothelin, and contributing to the development of the first non-peptide endothelin receptor antagonist (Clozel et al. 1993, Nature, 365, 759-761). The award of a British Heart Foundation Intermediate Fellowship  allowed Gillian to come to the University of Edinburgh to initiate her own research focussed on investigation of endothelin receptors in heart failure. Gillian took up a lectureship in Pharmacology in 1995 and moved to the BHF/University Centre for Cardiovascular Science, Queens Medical Research Institute in 2005 where she is currently a Reader in Cardiovascular Pharmacology.

Education/Academic qualification

Doctor of Philosophy (PhD), 'Studies in endotoxin shock with particular reference to vascular reactivity', University of Strathclyde

Award Date: 1 Jan 1989

Bachelor of Science, Investigation of the hypothermic effects of delta 9 tetrahydrocannabidiol, University of Aberdeen

Award Date: 1 Jan 1985

Keywords

  • RM Therapeutics. Pharmacology
  • cardiovascular
  • myocardial infarction
  • macrophage polarisation
  • Glucocorticoid
  • estrogen
  • angiogenesis
  • fibroblast
  • hydrogen sulphide
  • repair
  • regeneration
  • neutrophil
  • injury

Fingerprint

Dive into the research topics where Gillian Gray is active. These topic labels come from the works of this person. Together they form a unique fingerprint.
  • 1 Similar Profiles

Network

Recent external collaboration on country/territory level. Dive into details by clicking on the dots or