Robert Gros, Scientist, Vascular Biology Research Group; Assistant Professor, Departments of Physiology & Pharmacology and Medicine
Why I Became a Scientist
As a kid I always enjoyed playing with my chemistry set and my microscope, but being at the hospital and visiting my Oma when she suddenly died of cardiac arrest due to diabetic complications was one of those moments that really ignited the fire to pursue a career in medical research.
Research Summary
The focus of my laboratory is to investigate the cellular and molecular mechanisms involved in the regulation of vascular and cardiac function. In particular, we are interested in the role and regulation of G-protein-coupled receptor signaling pathways in both vascular smooth muscle cell and endothelial cell function under physiological and pathological conditions such as high blood pressure (hypertension) and diabetes.
The regulation of vascular and cardiac function is complex and involves many different signaling pathways, including the large family of G-protein-coupled receptors (GPCRs) and adenylyl cyclases, . We and other have identified that impaired function in these signaling pathways is associated with hypertension and heart disease. This impairment in GPCR-mediated function is in part due to increased expression/ function of G-protein-coupled receptor kinases. However, the cellular/molecular mechanism(s) involved in the regulation of altered GRK expression during the hypertensive state (or other pathological conditions) is unknown and is the focus of my laboratory’s research effort.
Research Questions and Disease Implications
Understanding the regulation of G-protein-coupled receptor kinases (GRKs) in cardiovascular disease.
The function of G-protein-coupled receptors is altered in diseases such as high blood pressure and heart disease. These diseases are associated with higher expression levels of GRKs, but why and how these levels are increased in unknown.
Identification of novel vascular G-protein-coupled receptor signaling pathways under physiological and patho-physiological conditions.
The rapid vascular actions of steroid hormones such as estrogen and aldosterone are in part mediated by a recently discovered G-protein-coupled receptor, GPR30. The vascular actions of steroid hormones have been implicated in both hypertension and heart disease. However, the role of GPR30 and its signalling pathways in cardiovascular disease in unknown.
Understanding the role of different adenylyl cyclase isoforms in cardiovascular regulation.
Adenylyl cyclase plays a critical role in the function and regulation of many different cell types, including blood vessel and heart cells. We have recently identified that different adenylyl cyclase isoforms have distinct roles in regulating cellular function. Additionally, we have recently identified a variant (polymorphism) of adenylyl cyclase isoform VI, which is associated with alterations in blood pressure and heart rate regulation in human subjects. What role this variant plays in cardiovascular disease development or progression is unknown.
Education
• Ph.D., Pharmacology, The University of Western Ontario, London, Ontario
Training
• Toronto General Hospital, University of Toronto, Toronto, Ontario
• Robarts Research Institute, London, Ontario
Awards
• New Investigator Award, Canadian Hypertension Society/Biovail,
• The Dr. Maureen Andrew New Investigator Award, Heart and Stroke Foundation of Ontario
• New Investigator Award, Heart and Stroke Foundation of Canada
• The Evelyn McGloin Fellowship, Heart and Stroke Foundation of Ontario
• Fellowship Award , Heart and Stroke Foundation of Ontario
• The Edward Christie Stevens Fellowship in Medicine. Faculty of Medicine, University of Toronto
• Graduate Studentship Award, Canadian Hypertension Society/Pfizer/MRC
• Summer Student Research Scholarship in Medicine, PMAC/MRC
Publications
• Gros, R., Van Uum, S., Ding, QM, Pickering, JG., Hegele, RA. and Feldman, RD. Enhanced function and a lean phenotype associated with a single nucleotide variant of human adenylyl cyclase 6. Arteriosclerosis, Thrombosis and Vascular Biology, 2007 Dec;27(12):2657-63.
• Gros, R, Ding, QM., Armstrong, S., O’Neil, C., Pickering, JG. and Feldman, RD. Rapid Effects of Aldosterone on Clonal Human Smooth Muscle Cells. American Journal of Physiology: Cell Physiology, 2007; 292(2):C788-94.
• Gros, R., Ding, QM., Chorazyczewski, J., Andrews, J., Pickering, JG., Hegele, RA. And Feldman, RD. The impact of blunted beta-adrenergic responsiveness on growth regulatory pathways in hypertension. Molecular Pharmacology. 2006;69(1):317-327.
• Feldman, RD and Gros, R. Defective Vasodilatory Mechanisms in Hypertension: a GPCR perspective. Current Opinion in Nephrology and Hypertension. 2006;15(2):135-40.
• Choi, J., Chiang, A., Taulier, N., Gros, R., Parini, A. and Husain, M. A calmodulin binding site on cyclin-E mediates Ca2+-sensitive G1/S transition in vascular smooth muscle cells. Circulation Research 2006;98:1273-1281.
• Gros, R#, Ding, QM#, Chorazyczewski, J., Pickering, JG., Limbird, L. and Feldman, RD. Adenylyl cyclase isoform-selective regulation of vascular smooth muscle proliferation and cytoskeletal re-organization. Circulation Research, 2006 Oct 13;99(8):845-52.
• Gros, R., Ding QM., Cao, H., Main, T., Hegele, RA. And Feldman, RD. Identification of a Dysfunctional Missense Single Nucleotide Polymorphism of Human Adenylyl Cyclase VI. Clinical Pharmacology & Therapeutics. 2005; 77(4):271-278.
Contact Information
Mellonie Carnahan, Administrative Assistant
Vascular Biology Group
Robarts Research Institute
Box 5015, 100 Perth Drive
London, ON N6A 5K8
Tel: 519-931-5777 x24118
email: mcarnahan@robarts.ca