Niall Macquaide

Dr Niall Macquaide graduated from Glasgow University in 2001 with a BSc (hons) in Physiology. He then went on to study for a PhD with Prof. Godfrey Smith in Glasgow. This used experimental and computer modelling techniques to study spontaneous Ca²⁺ release in cardiac myocytes. His postdoctoral work examined the electrophysiological remodelling which occurs through the progression of heart failure in a rabbit model of myocardial infarction. Through this work he built collaborative links with the lab of Prof Donald Bers in UC Davis, California. In 2009 he attained an EU Marie Curie Fellowship to work in Leuven, Belgium in the Lab of Karin Sipido to study alterations in ryanodine receptor (RyR) cluster organisation after remodelling in atrial fibrillation, acquiring new skills in skills in Super Resolution Microscopy. In 2013 he returned to Glasgow after being awarded a BHF intermediate research fellowship and an EU Marie Curie reintegration grant studying RyR cluster morphology in disease.

Current Research

Dr MacQuaide’s research focuses on the functional alterations in cardiac cells after remodelled in heart disease. He uses advanced imaging methodologies and analysis methods, to study Ca²⁺ subcellular Ca²⁺ release in living cells as well as super resolution microscopy to quantify alterations in the organisation of cellular proteins.

Ryanodine Receptor clustering. Using super resolution microscopy methods, he will measure clustering of ryanodine receptors (RyRs) with single protein accuracy and assess changes coincident with pathological remodelling following myocardial infarction (MI). Further detail on the mechanism of RyR clustering will be investigated in a cell line along with my collaborators in New Zealand (Dr Peter Jones) and Oslo (Dr Bill Louch). The goal here is to assess the changes which occur in failing hearts, how this can lead to an arrhythmogenic phenotype and to determine novel therapeutic strategies.

Ca2+-calmodulin-dependant kinease (CaMKII). CaMKII is shown to induce a “hyperphosphorylation” of RyR, with known pro-arrhythmogenic effects in MI. Genetically encoded probes will be used to assess CaMKII activity in in-vitro to assess the role this kinase in producing an arrhythmogenic phenotype. In collaboration with my collaborators: Prof Donald M Bers & Dr Julie Bossuyt, UC Davis, CA Dr Macquaide will determine how local Ca²⁺ gradients and CaMKII localisation may affect cellular function and changes in these activities within the context of pathological hypertrophic remodelling.

Atrial structural remodelling after MI. In collaboration with Dr. Anthony Workman (GU), investigation of structural alterations in patients with and without MI.

The role of PDE’s in the heart. In collaboration with Prof George Baillie (GU), the role of PDEs in the regulation of RyR and SERCA/ phospholamban (PLB) will be assessed. This new information will allow development of more targeted therapies for patients with heart disease.

Cardiac electrophysiology. In collaboration with Prof Godfrey Smith and Dr Rachel Myles (GU), Dr MacQuaide will use patch clamp and optical voltage/calcium measurement methods, to investigating the intercommunication between surface ion channels and intracellular Ca²⁺ release. It is hoped this will allow further understanding of the physiology and pathophysiology of excitation contraction coupling.