Clinton Robbins

Clinton Robbins, PhD

A quarter of all deaths in Canada are caused by complications associated with cardiovascular disease. The main cause of vascular disease is atherosclerosis, or build-up of plaque in the arteries. Atherosclerosis is an inflammatory disease. One subset of inflammatory cells, macrophages, play an important role in atherosclerosis progression. How these cells gather in plaques, however, is not clear. Macrophages can appear in plaques through recruitment of their monocyte precursors from the bloodstream. Our recently published data shows macrophages also proliferate or divide locally within the plaque. We are currently pursuing three main research streams:
  • Investigating the role of lesional macrophage proliferation in atherosclerosis.
    Which process - monocyte influx or macrophage proliferation - is more important? What are the mechanisms that drive proliferation? How does the balance between the two processes change with co-morbidities and treatment? Does one process influence the other? Which of the two is the better therapeutic target? The answers to these question are likely to identify new therapeutic targets in treating atherosclerosis.
  • Determining the contribution of embryonic- versus bone marrow-derived macrophages in atherosclerosis.
    Some macrophages develop from hematopoietic stem cells, while others develop prior to birth and independent of the bone marrow. We ask the important question whether functional differences exist between these different macrophage populations and to what extent each population contributes to disease.
  • Determining the molecular mechanisms that regulate macrophage accumulation in atherosclerosis.
    In addition to growth factors, hematopoiesis is tightly controlled at the transcriptional level. One such transcription factor, c-Myb, has been demonstrated to play an important role in the survival, proliferation, and differentiation of hematopoietic cells. We are currently studying the role of c-Myb in regulating inflammation in atherosclerosis.
Cell. 2018 Jan 11;172(1-2):176-190.e19
Kaufmann E, Sanz J, Dunn JL, Khan N, Mendonça LE, Pacis A, Tzelepis F, Pernet E, Dumaine A, Grenier JC, Mailhot-Léonard F, Ahmed E, Belle J, Besla R, Mazer B, King IL, Nijnik A, Robbins CS, Barreiro LB, Divangahi M
Immunity. 2017 Nov 21;47(5):974-989.e8
Clemente-Casares X, Hosseinzadeh S, Barbu I, Dick SA, Macklin JA, Wang Y, Momen A, Kantores C, Aronoff L, Farno M, Lucas TM, Avery J, Zarrin-Khat D, Elsaesser HJ, Razani B, Lavine KJ, Husain M, Brooks DG, Robbins CS, Cybulsky M, Epelman S
Sci Rep. 2017 Aug 09;7(1):7653
Desai HR, Sivasubramaniyam T, Revelo XS, Schroer SA, Luk CT, Rikkala PR, Metherel AH, Dodington DW, Park YJ, Kim MJ, Rapps JA, Besla R, Robbins CS, Wagner KU, Bazinet RP, Winer DA, Woo M
JCI Insight. 2017 Jul 20;2(14):
Sivasubramaniyam T, Schroer SA, Li A, Luk CT, Shi SY, Besla R, Dodington DW, Metherel AH, Kitson AP, Brunt JJ, Lopes J, Wagner KU, Bazinet RP, Bendeck MP, Robbins CS, Woo M
Infect Immun. 2017 Jul 03;:
Elphinstone RE, Besla R, Shikatani EA, Lu Z, Hausladen A, Davies M, Robbins CS, Husain M, Stamler JS, Kain KC
Nat Immunol. 2017 May 18;18(6):705
Roufaiel M, Gracey E, Siu A, Zhu SN, Lau A, Ibrahim H, Althagafi M, Tai K, Hyduk SJ, Cybulsky KO, Ensan S, Li A, Besla R, Becker HM, Xiao H, Luther SA, Inman RD, Robbins CS, Jongstra-Bilen J, Cybulsky MI
Nat Immunol. 2016 Sep 26;
Roufaiel M, Gracey E, Siu A, Zhu SN, Lau A, Ibrahim H, Althagafi M, Tai K, Hyduk SJ, Cybulsky KO, Ensan S, Li A, Besla R, Becker HM, Xiao H, Luther SA, Inman RD, Robbins CS, Jongstra-Bilen J, Cybulsky MI
Circ Res. 2016 May 13;118(10):1454-6
Robbins CS, Besla R
Arterioscler Thromb Vasc Biol. 2016 May 12;
Shikatani EA, Chandy M, Besla R, Li CC, Momen A, El-Mounayri O, Robbins CS, Husain M
Circ Res. 2016 Feb 19;118(4):637-52
Cybulsky MI, Cheong C, Robbins CS

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Assistant Professor, Departments of Laboratory Medicine and Pathobiology and Immunology, University of Toronto