Through our previous genomic studies using human blood and atherosclerotic plaque tissue samples, we 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 current interest in oxidative stress and metabolism, which can affect inflammation and atherosclerosis, we are pursuing studies to examine their effect on the immune system using in vivo models. For example, we are interested in examining the mechanisms by which oxygen homeostasis may affect cardiovascular disease processes such as atherosclerosis.
| 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 |
| Biesecker, Leslie G; Mullikin, James C; Facio, Flavia M et al. (2009) The ClinSeq Project: piloting large-scale genome sequencing for research in genomic medicine. Genome Res 19:1665-74 |
