Through our genomic studies using human blood and atherosclerotic plaque tissue samples, we have identified a marker of atherosclerosis disease severity and a cholesterol-independent marker of statin treatment, which has been granted a use patent. We have also identified tristetraprolin zinc finger protein 36 (TTP) as a mediator of localized tissue inflammation important for inflammatory arthritis and atherosclerosis. With our interest in oxidative stress and metabolism which affect inflammation, a driver of atherosclerosis, we are pursuing studies to examine the effect of altered p53 signaling on the immune system using specific genetic models.

Project Start
Project End
Budget Start
Budget End
Support Year
4
Fiscal Year
2013
Total Cost
$401,732
Indirect Cost
Name
National Heart, Lung, and Blood Institute
Department
Type
DUNS #
City
State
Country
Zip Code
Kang, Ju-Gyeong; Sung, Ho Joong; Amar, Marcelo J et al. (2016) Low ambient oxygen prevents atherosclerosis. J Mol Med (Berl) 94:277-86
Zhuang, Jie; Ma, Wenzhe; Lago, Cory U et al. (2012) Metabolic regulation of oxygen and redox homeostasis by p53: lessons from evolutionary biology? Free Radic Biol Med 53:1279-85
Kang, Ju-Gyeong; Amar, Marcelo J; Remaley, Alan T et al. (2011) Zinc finger protein tristetraprolin interacts with CCL3 mRNA and regulates tissue inflammation. J Immunol 187:2696-701
Kang, Ju-Gyeong; Sung, Ho Joong; Jawed, Sarah I et al. (2010) FOS expression in blood as a LDL-independent marker of statin treatment. Atherosclerosis 212:567-70