We reasoned that the variety of blood cells which circulate throughout the body presented an ideal tissue for atherosclerosis studies for a number of reasons. They are easily accessible and include inflammatory cells such as monocytes which are critical elements in atherosclerosis;circulating blood cells are in contact with the diseased endovascular lumen and as such may serve as reporters;and the variety of blood cells has defined cell surface markers facilitating their purification to homogeneity for gene expression analysis. Through our studies using human blood and atherosclerotic plaque tissue samples, we identified the Finkel-Biskis-Jinkins osteosarcoma protooncogene (FOS) as a potential marker of atherosclerosis and tristetraprolin zinc finger protein 36 (TTP) as a mediator of atherosclerosis pathogenesis. We been performing translational studies on FOS as a potential cholesterol-independent marker of statin treatment using clinical samples obtained by both intramural and extramural collaboration. We have also continued examining the role of TTP in mediating inflammation and atherosclerosis through its interaction with various mRNA species in model systems.
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| 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 |
