Research Interests

Proteoglycans have been shown to play a critical role in the initiation of atherosclerosis due to their ability to bind atherogenic lipoproteins leading to retention in the artery wall, as outlined in the “response to retention hypothesis”. Research in Dr. Tannock's laboratory aims to identify the role of proteoglycans in the pathogenesis of complications of diabetes and obesity, including atherosclerosis and nephropathy. Current studies are using angiotensin II to regulate vascular proteoglycans in animal models of diabetes, obesity, and atherosclerosis. Related studies are examining the interaction between inflammatory mediators/ markers and vascular proteoglycans. Subjects with obesity, metabolic syndrome or diabetes have modest but chronic elevations in levels of the acute phase reactants C reactive protein (CRP) and serum amyloid A (SAA). Dr Tannock has recently demonstrated that SAA alters vascular proteoglycan synthesis in a pro-atherogenic manner, suggesting that the modest chronically elevated levels of SAA seen in obese individuals could mechanistically contribute to atherosclerosis development. In addition, recent research demonstrates that hyperlipidemia can adversely contribute to the development of diabetic nephropathy, a process that may be mediated via renal accumulation of lipoproteins. The role of renal proteoglycans in the development of diabetic nephropathy is another topic of investigation. A major focus of the lab is to identify the underlying mechanisms that regulate proteoglycan synthesis and subsequently influence proteoglycan-lipoprotein interactions. Results from these studies will advance our understanding of the mechanisms of atherosclerosis, and may identify novel therapeutic targets to decrease lipoprotein retention as a strategy to prevent complications of diabetes and obesity.