Anthony Albert is Professor of Cardiovascular Science, with a research focus on how ion channels and associated cell signalling mechanisms regulate the function of blood vessels.
His laboratory investigates how stimulation of receptors on the surface of endothelial (ECs) and vascular smooth muscle cells (VSMCs) cause opening of ion channels. These processes have a major role in controlling the function of blood vessels, and are involved in pathology associated with diseases such as hypertension, angina, stroke, and atherosclerosis. Drugs that alter these cellular pathways may therefore be useful future treatments for cardiovascular disease.
Professor Albert's research is funded by the British Heart Foundation. His research uses a number of experimental approaches to unravel cellular pathways coupling receptors and ion channels to blood vessel function: freshly isolated single ECs and VSMCs, cell culture, patch clamp electrophysiology, RT-PCR, co-immunoprecipitation, western blotting, proximity ligation assay, phospholipid dot-blot, cell signalling biosensors, confocal microscopy, shRNA/morpholino knockdown of proteins, blocking anti-ion channel antibodies, transgenic mice, wire myography.
Prof Albert joined St George's in 1998 as a postdoctoral researcher, working with Professor William Large, now Emeritus Professor of Pharmacology. Their work investigated the properties of transient receptor potential (TRP) channels in vascular smooth muscle cells. He was employed as Senior lecturer at George's in 2006, and promoted to Reader in Cell Physiology in 2013 and Professor of Cardiovascular Science in 2018.
Prof Albert graduated with a BSc in Human Biology from Oxford Brookes University (1990), and completed an MSc in Neuroscience at Edinburgh University (1991). He obtained his PhD in Neurophysiology from the Royal Free Hospital School of Medicine, University of London (1997), working in the laboratory of Professor Mike Spyer, investigating the effect of serotonin on vagal preganglionic neurones.
Current research projects
Cellular mechanisms coupling depletion of intracellular Ca2+ stores to activation of canonical transient receptor potential 1 (TRPC1) channels in VSMCs. Store-operated TRPC1 channels are proposed to regulate contractility, proliferation, and migration of VSMCs, however little is known how these ion channels are activated. This project is based on our novel findings that store depletion is coupled to STIM1 activation which stimulates the classical Gq/PLC/PKC pathway leading to channel opening. The project also investigates how channel opening or gating is achieved by interactions between PKC-dependent phosphorylation and binding of phosphatidyl 4,5-bisphosphate (PIP2) at TRPC1 channel proteins. (funded by two previous BBSRC project grants)
Effect of stimulating calcium-sensing receptors (CaSR) in the vasculature. Our data indicates that activation of CaSR present on ECs produce vasodilatation, which is likely to regulate blood pressure. This project investigates the CaSR-mediated cellular mechanisms, in particular the role of endothelial TRPV4/TRPC1 and TRPC3 channels, which are proposed to generate nitric oxide production and activate intermediate Ca2+-activated K+ channels to induce endothelium-dependent hyperpolarisation and vasodilatation. In addtion, we are studying the idea that CaSR-mediated vasodilatations are reduced in hypertension, using animal models of hypertension such as spontanous hypertensive rats. (currently funded by BHF PhD Studentship)
Role of myristoylated alanine-rich C kinase substrate (MARCKS) on vascular contractility. PIP2 has a central role in contraction of VSMCs, by acting as a substrate for PLC-mediated pathways and regulating many ion channels and exchangers. MARCKS is a PIP2-binding protein which is highly expressed in VSMCs, but their is currently no information on its role in regulating contractility. This project investigate the novel proposal that G-protein-coupled receptor mechanisms linked to activation of MARCKS causes increased PIP2 binding to voltage-gated Ca2+ channels (VGCCs) leading to greater channel activation, more Ca2+ influx, and vascular contractility. This project highlights the novel concept that VGCCs may also be activated by cellular mechanisms not related to membrane depolarisation. (currently funded by BHF Project grant)
Principal Investigator
British Heart Foundation 3 yr Project Grant. ‘Investigation of MARCKS-PIP2-voltage-gated Ca2+ channel pathway in vascular smooth muscle’, 01/02/19 to 31/01/22, (PG/18/69/33870), £191,659.
British Heart Foundation 3 yr PhD Studentship, ‘Investigations into calcium-sensing receptor mechanisms in the vasculature’, 01/10/17 to 30/09/20, (FS/17/40/32942), £130,820.
British Heart Foundation 3 yr PhD Studentship, ‘Role of PIP2-binding protein MARCKS on voltage-gated Ca2+ channels and vascular reactivity’, 01/10/15 to 30/09/18, (FS/15/44/31570), £114,469.
Biotechnology and Biological Sciences Research Council 3 yr Project Grant, ‘STIM1-mediated PLC activity and TRPC1 channel activation in vascular smooth muscle’, 01/07/15 to 30/04/19, (BB/M018350/1), £365,834.
British Heart Foundation 3 yr PhD Studentship. ‘Investigations into Calcium-sensing receptor mechanisms in the vasculature’, 01/09/13 to 31/08/16, (FS/13/1030021), £136,595.
Biotechnology and Biological Sciences Research Council 3 yr Project Grant. ‘Properties and function of TRPC proteins in vascular smooth muscle using transgenic mice’. 01/04/12 to 30/05/15, (BB/J007226/1), £367,568.
British Heart Foundation 3 yr Project Grant. ‘Study of the physiological functions of TRPC-mediated Ca2+-permeable cation conductances in arterial smooth muscle cells’, 01/01/08 to 30/06/11, (PG/07/079/23568), £194,564.
Co-applicant
British Heart Foundation, 3 yr project grant, IA Greenwood & AP Albert ‘Defining the role of phosphatidyl 4,5- bisphosphate on arterial calcium-activated chloride channels’, 01/07/14 to 31/06/17 (PG/14/57/30992), £189,585.
SWAN Alliance, 3 yr PhD studentship. IA Greenwood & AP Albert, ‘Properties of TMEM16A in vascular tissue’, 01/10/11-30/09/14, £65,000.
Arthritis Research UK, 2 yr project grant. TJ Chambers & AP Albert, ‘The role of Urocortin in the regulation of bone resorption’, 01/04/09 to 31/03/11, (18733), £181,684.
British Heart Foundation, 3 yr project grant. WA Large & AP Albert, ‘Investigation into the activation mechanisms of novel protein kinase C-dependent TRPC channel proteins in vascular smooth muscle cells’, 01/11/08 to 31/10/11, (PG/08/042/25066), £226,078.
Dr Yousif Shamsaldeen - Post-doctoral research assistant (BHF funded).
Simonette Carlton-Carew - PhD student (BHF funded).
Prof Albert is investigating TRPC channels in muscle cells from genetically-modified mice, developed to express non-working TRPC channel proteins. This work is in collaboration with Professor Lutz Birnhaumer, a leading expert in the field of ion channels and cell signalling, who is based in the Transmembrane Signaling Group at the National Institute of Environmental Health Sciences (NIEHS) in the USA, and Catholic University of Argentina.
Prof Albert collaborates with other researchers in the Biomedical Sciences Research Centre at St George's, including Professor Iain Greenwood (TMEM16A channels in vascular smooth muscle), and Vaneesa Ho (Calcium-sensing receptors in the vasculature).
Prof Albert is currently collaborating with Professor Ting Kang Nee, Department of Biomedical Sciences, Malaysia Campus, University of Nottingham, on a project investigating novel compounds involved in regulating calcium-permeable channels in the vasculature.
Prof Albert obtained a Postgraduate Certificate in Healthcare and Biomedical Education at St George's in 2008.
He gives lectures, tutorials, and expert forums on fundamentals of pharmacology, autonomic nervous system, and the cardiovascular system to MBBS5, MBBS4, BSc Healthcare Sciences, and MSc Physician Associate Studies students.
His current administrative roles are:
- MBBS5 Specialist lead for pharmacology and cardiovascular system
- MBBS5 Year 1 Life Support module lead
- Short-Course committee member
- Personal tutor to MBBS5 and MBBS4 students