Contact Information

Manon Levesque Departmental Secretary of Pathology and Laboratory Medicine
451 Smyth road,
Room 4155
Ottawa, Ontario
K1H 8M5

Telephone: 613-562-5422
Fax: 613-562-5442
Email: mlevesq2@uottawa.ca

Sheila Schnupp
Office and Residency Program Administrator (Anatomical)
Telephone: 613-562-5800 ext. 8342
Fax: 613-562-5442
Email: sschnupp@uottawa.ca

John P. Veinot, M.D., F.R.C.P.C (Canada)
Chairman, Department of Pathology and Laboratory Medicine
Tel: 613-562-5422
Fax: 613-562-5442
Email: sschnupp@uottawa.ca

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Yves L. Marcel, B.Sc. (Rouen), Ph.D. (Toulouse)

Yves L. Marcel

Professor
Department of Pathology and Laboratory Medicine and
Department of Biochemistry, Microbiology and Immunology
Faculty of Medicine.

Member
Faculty of Graduate and Postdoctoral Studies
University of Ottawa.

Director
Lipoproteins and Atherosclerosis Group
University of Ottawa Heart Institute.

Telephone: 613-761-5255
Fax: 613-761-5281
Email: ylmarcel@ottawaheart.ca

Research Interests

I demonstrated that the C-terminal domain of apoA-I participates in ABCA1-mediated lipid efflux (2002) and provided the first evidence for the essential contribution of hepatic ABCA1 to the lipidation of nascent HDL as well as exogenous apoA-I (Kiss, 2003). Wth J. Cohen and R. McPherson, we showed that multiple non-synonymous mutations in ABCA1 contribute to the low HDL phenotype (2004). Pursuing this work with R. McPherson (2005), we showed that efflux defects are frequent in low HDL syndrome and genetically heterogeneous. Furthermore, the monocyte-derived macrophages of these patients present with a pro-inflammatory phenotype that is independent of cholesterol efflux (Kiss, 2007; Sarov-Blat, 2007). This  indicates that differentiation of monocytes under condition of low HDL leads to the selection of inflammatory monocytes, a new parameter of the anti-inflammatory properties of HDL.

In macrophages I showed that SR-A and LDL receptor transport cholesterol through distinct pathways (Wang, 2006) and that efflux through HDL is significant contributor to reverse cholesterol transport (Wang, 2007). With R.S. Kiss (2005), I showed that GULP is an adaptor to LRP that controls the traffic of cholesterol to and out of the late endosomes through its effects on prosaposin and sphingolipid transport. Recently, I discovered that cathepsin D is a positive regulator of ABCA1 (Haidar, 2006) and demonstrated that NPC1 activity activates CTSD and subsequently ABCA1 in hepatocytes but not macrophages (Wang, 2007). We were also the first to demonstrate that reverse cholesterol transport from macrophages that do not express ABCA1 is impaired (Wang, 2007).

Recent Publications

  • Ouimet, M., Franklin, V., Mak, E., Liao, X., Tabas, I. and Marcel, YL. Autophagy regulates cholesterol efflux from macrophage foam cells via lysosomal acid lipase. Cell Metab. 13, 655-667.  June 8, 2011.
  • Weers PM, Patel AB, Wan LC, Guigard E, Kay CM, Hafiane A, McPherson R, Marcel YL, Kiss RS. Novel N-terminal mutation of human apolipoprotein A-I reduces self-association and impairs LCAT activation. J Lipid Res. 2011 Jan;52(1):35-44. Epub 2010 Sep 30.
  • Marcel YL, Ouimet M, Wang M-D Cellular lipid traffic and lipid transporters: Regulation of efflux and HDL formation. In Cellular Lipid Metabolism, C. Ehnholm, Ed. Springer. Pg 73-106, 2009.
  • Marcel YL, Ouimet M, Wang M-D Regulation of cholesterol efflux in macrophages. Curr. Opin. Lipidol.  2008, 19: 455-461.
  • Ouimet M, Wang MD, Cadotte N, Ho K, Marcel YL. Epoxycholesterol impairs cholesteryl ester hydrolysis in macrophage foam cells, resulting in decreased cholesterol efflux. Arterioscler Thromb Vasc Biol. 2008 Jun;28(6):1144-50. Epub 2008 Mar 27. PMID: 18369155 [PubMed - indexed for MEDLINE]
  • Wang M-D, Franklin V, Sundaram M, Kiss RS, Ho K, Gallant M, and Marcel YL. Differential regulation of ABCA1 expression and apoA-I lipidation by NPC1 in murine hepatocytes and macrophages. J. Biol. Chem. 2007 Aug 3;282(31):22525-33. Epub 2007 Jun 5.
  • Wang M-D, Franklin V, and Marcel YL. In vivo reverse cholesterol transport from macrophages lacking ABCA1 expression is impaired. Arterioscler Thromb Vasc Biol. 2007 Aug;27(8):1837-42. Epub 2007 May 31.
  • Sarov-Blat L, Kiss RS, Haidar B, Kavaslar N, Jaye M, Bertiaux M, Steplewski K, Hurle MR, Sprecher D, McPherson R, and Marcel YL Predominance of a proinflammatory phenotype in monocyte-derived macrophages from subjects with low plasma HDL-cholesterol ATVB published February 22, 2007, 10.1161
  • Kiss RS, Kavaslar N, Okuhira KI, Freeman MW, Walter S, Milne RW, McPherson R, and Marcel YL.Genetic Etiology of Isolated Low HDL Syndrome: Incidence and Heterogeneity of Efflux Defects. ATVB published February 15, 2007, 10.1161
  • Wang MD, Kiss RS, Franklin V, McBride HM, Whitman SC, Marcel YL.  Different intracellular trafficking of LDL- and acetylated LDL-derived cholesterol lead to distinct reverse cholesterol transport mechanisms. J Lipid Res. 2006 Dec 5; [Epub ahead of print]
  • Kiss RS, Elliott MR, Ma Z, Marcel YL, Ravichandran KS.  Apoptotic cells induce a phosphatidylserine-dependent homeostatic response from phagocytes. Curr. Biol. 2006 Nov 21;16(22):2252-8.
  • Haidar B, Kiss RS, Sarov-Blat L, Brunet R, Harder C, McPherson R, Marcel YL. Cathepsin D, a lysosomal protease, regulates ABCA1-mediated lipid efflux. J Biol Chem. 2006 Dec 29;281(52):39971-81. Epub 2006 Oct 10.
  • Kiss RS, Ma Z, Nakada-Tsukui K, Brugnera E, Vassiliou G, McBride HM, Ravichandran KS, Marcel YL. The lipoprotein receptor-related protein-1 (LRP) adapter protein GULP mediates trafficking of the LRP ligand prosaposin, leading to sphingolipid and free cholesterol accumulation in late endosomes and impaired efflux. J Biol Chem. 2006 Apr 28;281(17):12081-92. Epub 2006 Feb 22.

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