Choy Lab

Research in my laboratory is focused on understanding the mechanisms by which T cells and inflammatory responses become inappropriately activated in disease settings and how this causes organ damage. 

Immune responses that cause organ transplant rejection and autoimmune diseases

Research in my laboratory is focused on understanding how the immune system is activated towards transplanted organs and how it causes resultant rejection. We have provided particular attention to how innate immune signals, such as cytokines secreted by innate immune cells and vascular cells, control the activation of T cells and how the gut microbiota influences immune responses that cause organ transplant rejection.  Studies are also investigating cell engineering approaches that protect blood vessels in transplanted organs and how this can be applied to prevent rejection.

Nitric oxide signaling and production

Nitric oxide (NO) is a bioactive gas that controls many cell biological responses. Dysregulation of its production and/or bioactivity is involved in many diseases. My laboratory is interested in understanding how NO effects cell signaling and how its production is controlled by NO synthases. The role of NO and NO synthases in cell biology and immune responses is also being studied.

Email: 

JONATHAN CHOY
jonathan_choy@sfu.ca

LAB ROOM: 

TASC II 8130 

LAB PHONE:

(778) 782-8707

Selected Publications

  • Granville DJ, Cassidy BA, Ruehlmann DO, Choy JC, Brenner C, Kroemer G, van Breemen C, Margaron P, Hunt DW, McManus BM. (2001) Mitochondrial release of apoptosis inducing factor and cytochrome c during smooth muscle cell apoptosis. Am J Pathol. 159: 305-311
  • Choy JC, Granville DJ, Hunt DWC, McManus BM. (2001) Endothelial cell apoptosis: Biochemical characteristics and potential implications for atherosclerosis.  J Mol Cell Cardiol. 33: 1673-90
  • Granville DJ, Ruehlmann DO, Choy JC, Cassidy BA, Thompson CB, van Breemen C, McManus BM. (2001) Bcl-2 increases emptying of endoplasmic reticulum Ca2+ stores during photodynamic therapy-induced apoptosis. Cell Calcium. 30(5):343-50
  • Singaraja RR, Fievet C, Castro G, James ER, Hennuyer N, Clee SM, Bissada N, Choy JC, Fruchart JC, McManus BM, Staels B, Hayden MR. (2002) Increased ABCA1 activity protects against atherosclerosis. J Clin Invest. 110(1):35-42

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