Neurology &
Neurological Sciences
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Welcome To Huang Lab

Our research is focused on the role of redox balance in tissue maintenance and repair.  Under normal metabolic conditions, oxygen free radicals are generated as by-products from oxidative phosphorylation in the mitochondria and from normal biochemical reactions in the cytosol.  Oxygen free radicals are highly reactive, hence the name reactive oxygen species (ROS), and can cause damages to macromolecules, such as DNA, RNA, lipids, and proteins.  To protect important macromolecules and organelles from ROS-mediated damages, we are equipped with antioxidant enzymes and small reducing molecules to remove ROS.  However, low levels of ROS are also needed to control redox-sensitive proteins involved in various biochemical pathways.  One example is the transient inactivation of protein tyrosine phosphatases by oxidation or alkylation of the active site Cysteine to facilitate signal transduction.  The balance between the removal and production of ROS determines the reduction and oxidation (redox) status in tissues, cells, and subcellular compartments.  Just as microclimate is prevalent in the Bay area, regional differences in redox balance is common and shapes localized changes in cell proliferation and tissue maintenance.

Under pathological conditions, such as infection or inflammation, the production of ROS exceeds the antioxidant capacity, and tips the redox balance to causing cell death and tissue dysfunction.  Exposure to external stressors, such as toxic chemicals or irradiation, can also cause immediate damage and sustained alteration in redox balance in tissues and cells.  To determine how changes in redox balance affect tissue maintenance and repair, we use tissue culture cells and mouse models with altered antioxidant capacity and subject these experimental models to various forms of oxidative stress. We then determine the shift in redox homeostasis, identify the biochemical pathways affected by the condition, quantify the resulting cell death/tissue damage, and determine the long-term consequences of redox imbalance.  Currently our studies are focused on two areas:

1. Redox-balance and irradiation-mediated changes in hippocampal neurogenesis and the associated changes in hippocampal-mediated learning and memory.

2. Redox balance and chronic HCV infection (with or without alcohol exposure)-mediated changes in redox-sensitive proteome in the liver and the associated changes in liver histopathology.

 

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