B. Medicine, 1986
Ph.D. Neuroscience, 1991
Position: Associate Professor
Office: (604) 875-2000 ext 4726
Fax: (604) 875-3871
My research is on the mechanism of action of mood stabilizing
drugs at molecular and cellular levels, with focus on the neuroprotective
effects of these drugs against oxidative stress. Previously,we found that
mood stabilizing drugs prevented oxidative damage and upregulated
glutathione (GSH)/glutathione S-transferase (GST) detoxification pathway. My
research objective is to understand the role of GSH/GST pathway in the
pharmacological treatment of mood stabilizing drugs. Research aims are: 1)
to examine if GSH and GST mediate the neuroprotective effects of mood
stabilizing drugs against oxidative damage; 2) to determine the role of Nrf2
transcription factor in GSH/GST pathway regulated by mood stabilizing drugs;
3) to identify oxidative modifications of synaptic proteins and 4) to
determine role of GSH/GST pathway in mood stabilizing treatment using animal
models for depression and mania. This study will lead to identifying new
therapeutic targets in the GSH/GST pathway for investigation in clinical trials in the near future,
contributing to new and more effective therapies for bipolar disorder
with fewer side effects.
Research techniques employed in my work include cell culturing,
measurement of lipid peroxidation and protein oxidation, TUNEL staining, real
time-PCR,DNA cloning, in vitro transcription and translation, cell
transfection,immunoblotting analysis, co-immunoprecipitation,
immunohistochemistry, electrophoretic mobility shift assay, locomotor
activity analysis and forced swim test among others.
- Andreazza AC, Shao L, Wang JF and Young LT (2010). Decreased mitochondrial complex I activity and increased oxidative damage to mitochondrial proteins in the prefrontal cortex of patients with bipolar disorder. Archives of General Psychiatry, 67: 360-8.
- Gawryluk JW, Wang JF, Andreazza AC, Shao L, Young LT. (2010) Decreased
levels of glutathione, the major brain antioxidant, in post-mortem
prefrontal cortex from patients with psychiatric disorders. Int J
Neuropsychopharmacol. 16: 1-8.
- Wang JF, Shao L, Sun X and Young LT (2009). Increased oxidative stress in
anterior cingulate cortex of subjects with bipolar disorder and
schizophrenia. Bipolar disorders, 11: 523-529
- Shao L, Cui J, Young LT and Wang JF (2008). The effect of mood stabilizer
lithium on expression and activity of glutathione-S-transferase isoenzymes.
Neuroscience, 151: 518-24.
- Wang JF (2007). Defects of mitochondrial electron transport chain in
bipolar disorder: implications for mood stabilizing treatment. Canadian
Journal of Psychiatry,52: 753-62. (Review)
- Cui J, Shao L, Young LT and Wang JF (2007). Role of glutathione in
neuroprotective effects of mood stabilizing drugs lithium and valproate.
Neuroscience, 144: 1447-53.
- Shao L, Sun X, Xu L, Young LT and Wang JF (2006). Mood stabilizing drug
lithium increases expression of endoplasmic reticulum stress proteins in
primary cultured rat cerebralcortical cells. Life Science, 78: 1317-23.
- Sun X, Wang JF, Tseng M and Young LT (2006). Down regulation in
components of mitochondrial electron transport chain in post-mortem frontal
cortex from subjects with bipolar disorder. Journal of Psychiatry and
Neuroscience, 31: 189-96.
- Shao L, Young LT and Wang JF (2005). Chronic treatment with mood
stabilizers lithium and valproate prevents excitotoxicity by inhibiting
oxidative stress in rat cerebral cortical cells. Biological Psychiatry, 58: 879-84.
- Wang JF, Shao L, Sun X, Young LT (2004). Glutathione S-transferase is a
novel target for mood stabilizing drugs in primary cultured neurons. Journal
of Neurochemistry. 88: 1477-84.