McMaster University

McMaster University



Bernardo Trigatti

Bernardo Trigatti, PhD

Biochemistry and Biomedical Sciences

David Braley Cardiac, Vascular, and Stroke Research Institute
Hamilton General Hospital Campus
905-521-2100 ext. 40744


  • Cell Biology and Regulation

Molecular mechanisms of atherosclerosis development

Atherosclerosis is a major cause of heart disease and stroke, among the leading causes of hospitalization and death in Western countries. It is a multifactorial disease involving a variety of physiological pathways. These include innate immunity, inflammation and lipoprotein metabolism.

Our laboratory utilizes mouse molecular genetics to delineate the contribution of components of these pathways to the development of atherosclerosis. The mouse has been an extremely useful model genetic system to analyze pathways involved in atherosclerosis. In conventional mouse models of atherosclerosis, including the workhorse apoE and LDL receptor knockout mouse strains, atherosclerosis develops primarily in the aorta while coronary arteries, which feed the heart, appear resistant to disease. In contrast, mice that lack a receptor for high density lipoproteins develop extensive atherosclerosis in their coronary arteries as well as increased atherosclerosis in their aortas. These mice develop myocardial infarction as a result of the extensive coronary artery atherosclerosis. This suggests that the HDL receptor, called SR-BI, plays a key role in protection against coronary artery atherosclerosis. One of the main focuses of the lab is to delineate the mechanisms by which expression of SR-BI in bone marrow derived cells including macrophages, protects against atherosclerosis. In particular, we are interested in understanding the role of this receptor in lipid transport as well as cell signalling.

We are also making use of our mouse models of coronary artery atherosclerosis to delineate the factors that normally contribute to the resistance of mouse coronary arteries to atherosclerosis development, as well as to test the contribution of different physiological pathways to the development of coronary artery atherosclerosis and myocardial infarction.3

Selected Publications

  • Braun, A. , Rigotti, A. and Trigatti, B.L. (2008) Myocardial infarction following atherosclerosis in murine models. Curr Drug Targets. 9:217-23.
  • Minahk,C, Kim,KW, Nelson,R, Trigatti, BL, Lehner, R and Vance, DE. (2008) Conversion of Low Density Lipoprotein-Associated Phosphatidylcholine to Triacylglycerol by Primary Hepatocytes. Journal of Biological Chemistry 283:6449-6458
  • Zhang Y, Ahmed AM, Tran T, Lin J, McFarlane N, Boreham DR, Igdoura SA, Truant R, Trigatti BL. (2007) Inhibition of endocytosis affects HDL-lipid uptake mediated by the human scavenger receptor class B type I. Molecular Membrane Biology 24:442-454.
  • Zhang Y, Ahmed AM, McFarlane N, Capone C, Boreham DR, Truant R, Igdoura SA, Trigatti BL. (2007) Regulation of SR-BI-mediated selective lipid uptake in Chinese hamster ovary-derived cells by protein kinase signaling pathways. Journal of Lipid Research 48:405-416
  • Karackattu SL, Trigatti B, Krieger M (2006) Hepatic Lipase Deficiency Delays Atherosclerosis, Myocardial Infarction, and Cardiac Dysfunction and Extends Lifespan in SR-BI/Apolipoprotein E Double Knockout Mice. Arterioscler Thromb Vasc Biol. 26:548-554.
  • SD. Covey, M Krieger, W Wang, M Penman, and BL. Trigatti (2003) Scavenger Receptor Class B Type I-Mediated Protection Against Atherosclerosis in LDL Receptor-Negative Mice Involves Its Expression in Bone Marrow-Derived Cells. Arteriosclerosis, Thrombosis and Vascular Biology 23: 1589-1594.
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