What We Do
The Trigatti Lab is part of the Department of Biochemistry and Biomedical Sciences at McMaster University and the Thrombosis & Atherosclerosis Research Institute of McMaster University and Hamilton Health Sciences in Hamilton, Ontario, Canada.
Our research is focused on the molecular mechanisms involved in the development of atherosclerosis, a chronic inflammatory disease characterized by the development of cholesterol-rich plaques in the arteries. Atherosclerosis is one of the major causes of coronary heart disease and a leading cause of hospitalization and death worldwide. Using mouse molecular genetics, we aim to determine and characterize the contributions of a variety of physiological pathways involved in atherosclerotic development and resulting cardiovascular disease.
Our research is supported by:
Heart & Stroke and Canadian Institutes of Health Research.
Who We Are
Principal Investigator
Bernardo Trigatti
BSc, PhD
Professor, Department of Biochemistry and Biomedical Sciences
Postdoctoral Fellows
Graduate Students
Undergraduate Students
Former Lab Members
Yak Deng
BSc
Research Technician
Research
Atherosclerosis is a multifactorial disease driven by interactions between circulating lipoproteins, inflammatory cells and cells of the arterial wall. The disease results from dysregulated lipid metabolism and inflammation. Circulating low density lipoproteins (LDL) may be retained in the artery wall and chemically modified, triggering an inflammatory response resulting in the recruitment of monocytes. The monocytes are subsequently differentiated into macrophage foam cells, characterized by a buildup of cholesterol in the cytoplasm from the uptake of modified lipoproteins. The foam cells comprise fatty streaks in the arterial intima and develop into atherosclerotic plaque as the disease progresses. In late stages of atherosclerosis, a necrotic core forms in the plaque as a result of high rates of macrophage cell death and the defective clearance of dead cells. A large, lipid-rich necrotic core destabilizes the atherosclerotic plaque leading to plaque rupture, causing the formation of a thrombus and potentially leading to ischemia.
High density lipoproteins (HDL) counter the development of atherosclerosis through mediating reverse cholesterol transport, a process through which cholesterol is removed from the foam cells of the atherosclerotic plaque. HDL transports the cholesterol to the liver where hepatocytes secrete the cholesterol into the bile for reuptake or disposal. Reverse cholesterol transport is driven by ATP binding cassette transporters (ABCA1 and ABCG1) in macrophages and by the HDL receptor, scavenger receptor class B type 1 (SR-B1) in the liver. HDL also protects against atherosclerosis by activating signaling pathways in cells (like macrophages and endothelial cells) in the artery wall leading to atheroprotective responses.
In the Trigatti Lab, we are interested in investigating molecular pathways that drive the development of atherosclerosis. In particular, our ongoing projects focus on the role of the HDL receptor SR-B1 in protection against atherosclerosis in coronary arteries, the role of HDL signaling in modulating cell death within atherosclerotic plaques, other molecular pathways that modulate atherosclerosis development and the role of signaling by HDL in cardiomyocytes in protecting against cardiotoxicity.
Current Research
Learn more about our research focuses.
Publications
Recent Publications
Fuller, M.T., Dadoo, O., Xiong, T., Chivukula, P., MacDonald, M.E., Lee, S.K., Austin, R.C., Igdoura, S.A., and Trigatti, B.L. (2022). Extensive diet-induced atherosclerosis in scavenger receptor class B type 1-deficient mice is associated with substantial leukocytosis and elevated vascular cell adhesion molecule-1 expression in coronary artery endothelium. Front Physiol 13, 1023397. 10.3389/fphys.2022.1023397.
Kluck, G.E.G., Qian, A.S., Sakarya, E.H., Quach, H., Deng, Y.D., and Trigatti, B.L. (2023). Apolipoprotein A1 Protects Against Necrotic Core Development in Atherosclerotic Plaques: PDZK1-Dependent High-Density Lipoprotein Suppression of Necroptosis in Macrophages. Arteriosclerosis, Thrombosis, and Vascular Biology, 43, 45–63. doi: 10.1161/ATVBAHA.122.318062
Kluck, G.E.G., Yoo, J. A., Sakarya, E.H., and Trigatti, B.L. (2021). Good Cholesterol Gone Bad? HDL and COVID-19. International Journal of Molecular Sciences, 22, 10182. doi:10.3390/ijms221910182
Xiong, T., Qian, A.S., and Trigatti, B.L. (2021). The local effects of proprotein convertase subtilisin/kexin type 9 (PCSK9) on the inflammatory atheroma: beyond LDL cholesterol lowering. Vessel Plus, 5(5). doi: 10.20517/2574-1209.2020.71
Kluck, G.E.G, Durham, K. K., Yoo, J. A., & Trigatti, B. L. (2020). High Density Lipoprotein and Its Precursor Protein Apolipoprotein A1 as Potential Therapeutics to Prevent Anthracycline Associated Cardiotoxicity. Frontiers in cardiovascular medicine, 7, 65. doi: 10.3389/fcvm.2020.00065
Rodriguez, A., Trigatti, B. L., Mineo, C., Knaack, D., Wilkins, J. T., Sahoo, D., Asztalos, B. F., Mora, S., Cuchel, M., Pownall, H. J., Rosales, C., Bernatchez, P., Ribeiro Martins da Silva, A., Getz, G. S., Barber, J. L., Shearer, G. C., Zivkovic, A. M., Tietge, U., Sacks, F. M., Connelly, M. A., … Martel, C. (2019). Proceedings of the Ninth HDL (High-Density Lipoprotein) Workshop: Focus on Cardiovascular Disease. Arteriosclerosis, thrombosis, and vascular biology, 39(12), 2457–2467. doi: 10.1161/ATVBAHA.119.313340
Sokeechand, B., & Trigatti, B. L. (2019). Un-JAMming atherosclerotic arteries: JAM-L as a target to attenuate plaque development. Clinical science (London, England : 1979), 133(14), 1581–1585. doi: 10.1042/CS20190541
Durham, K. K., Kluck, G.E.G, Mak, K. C., Deng, Y. D., & Trigatti, B. L. (2019). Treatment with apolipoprotein A1 protects mice against doxorubicin-induced cardiotoxicity in a scavenger receptor class B, type I-dependent manner. American journal of physiology. Heart and circulatory physiology, 316(6), H1447–H1457. doi: 10.1152/ajpheart.00432.2018
Gonzalez, L., MacDonald, M. E., Deng, Y. D., & Trigatti, B. L. (2018). Hyperglycemia Aggravates Diet-Induced Coronary Artery Disease and Myocardial Infarction in SR-B1-Knockout/ApoE-Hypomorphic Mice. Frontiers in physiology, 9, 1398. doi: 10.3389/fphys.2018.01398
Yu, P., Qian, A. S., Chathely, K. M., & Trigatti, B. L. (2018). Data on leukocyte PDZK1 deficiency affecting macrophage apoptosis but not monocyte recruitment, cell proliferation, macrophage abundance or ER stress in atherosclerotic plaques of LDLR deficient mice. Data in brief, 19, 1148–1161. doi: 10.1016/j.dib.2018.05.128
Yu, P., Qian, A. S., Chathely, K. M., & Trigatti, B. L. (2018). PDZK1 in leukocytes protects against cellular apoptosis and necrotic core development in atherosclerotic plaques in high fat diet fed ldl receptor deficient mice. Atherosclerosis, 276, 171–181. doi: 10.1016/j.atherosclerosis.2018.05.009
Durham, K. K., Chathely, K. M., & Trigatti, B. L. (2018). High-density lipoprotein protects cardiomyocytes against necrosis induced by oxygen and glucose deprivation through SR-B1, PI3K, and AKT1 and 2. The Biochemical journal, 475(7), 1253–1265. doi: 10.1042/BCJ20170703
Yu, P., Xiong, T., Tenedero, C. B., Lebeau, P., Ni, R., MacDonald, M. E., Gross, P. L., Austin, R. C., & Trigatti, B. L. (2018). Rosuvastatin Reduces Aortic Sinus and Coronary Artery Atherosclerosis in SR-B1 (Scavenger Receptor Class B Type 1)/ApoE (Apolipoprotein E) Double Knockout Mice Independently of Plasma Cholesterol Lowering. Arteriosclerosis, thrombosis, and vascular biology, 38(1), 26–39. doi: 10.1161/ATVBAHA.117.305140
Durham, K. K., Chathely, K. M., Mak, K. C., Momen, A., Thomas, C. T., Zhao, Y. Y., MacDonald, M. E., Curtis, J. M., Husain, M., & Trigatti, B. L. (2018). HDL protects against doxorubicin-induced cardiotoxicity in a scavenger receptor class B type 1-, PI3K-, and Akt-dependent manner. American journal of physiology. Heart and circulatory physiology, 314(1), H31–H44. doi: 10.1152/ajpheart.00521.2016
For a complete list of publications, please visit PubMed.
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Contact
Information Box Group
Bernardo Trigatti
BSc, PhD
Professor, Department of Biochemistry and Biomedical Sciences
Interested graduate students and postdoctoral fellows are encouraged to send Dr. Trigatti a cover letter with a statement of interest, a curriculum vitae (CV), a transcript/grade report and two recommendation letters from faculty members familiar with the research background of the student.
Further McMaster information and resources
Prospective graduate students may consult the following websites for entrance requirements and admissions information:
- School of Graduate Studies
- Faculty of Health Sciences Graduate Studies
- Biochemistry Graduate Program
- Medical Sciences Graduate Program