Sangderk Lee, Ph.D.

Bio / Education: 


1990. 3-1994. 2: B.S. College of Pharmacy, Seoul National University, Seoul, S. Korea.
1994. 3-1996. 2: M.S. College of Pharmacy, Seoul National University, Seoul, S. Korea.
2002. 9-2006. 5: Ph.D. of Pharmacology, University of Virginia School of Medicine, Charlottesville, VA.
2006. 5-2011. 8: Postdoctoral Fellow, Pathology & Medicine-Cardiology, UCLA School of Medicine, Los Angeles, CA.


2011. 9-2013. 5: Assistant Researcher at Dept. Pathology & Laboratory Medicine, UCLA
School of Medicine, Los Angeles, CA.
2013. 6-present: Assistant Professor (Tenure-Track) at Saha Cardiovascular Research Center, Dept.
Pharmacology & Nutritional Sciences, University of Kentucky, Lexington, KY.

Research Description: 

My research goal is to identify mechanism of the development of hyperlipidemia-associated cardiovascular diseases and find therapeutic targets to prevent or delay progress of the diseases. Hyperlipidemia-induced oxidative stress and accumulation of 'oxidized phospholipids' in the vessel wall are key events for the development of chronic inflammatory vascular diseases including atherosclerosis and aneurysm. These vascular diseases are accompanied by inflammatory cytokine overexpression and infiltration of monocytes and macrophages into the vessel wall. Oxidized phospholipids, as represented by Ox-PAPC, strongly activates vascular endothelial cells for the expression of proinflammatory and prothrombotic gene expressions. First, we test the hypothesis that the oxidized phospholipids employ both receptor and non-receptor cytosolic signaling and epigenetic modification for the induction of proinflammatory and prothrombotic gene expressions in the vascular endothelium. For study, we employ in vitro cell system and in vivo mouse model system (LDLR or ApoE null) with biochemical and epigenetics approaches to find key regulatory pathway and pharmacological targets. The elevation of ApoB-containing lipoproteins (VLDL and LDL) in the blood stream is a risk factor for the development of atherosclerosis and aneurysm. As second lab project, we study the role of 'heparin binding epidermal growth factor-like growth factor (HB-EGF)' signaling in regulating lipid balance in the liver and blood circulation. We hypothesize that HB-EGF is an unappreciated regulator of hepatic lipoprotein production/secretion and a potential target for lipid-lowering in circulation. HB-EGF targeting using anti-sense oligonucleotide (ASO) approach showed remarkable suppression of both hyperlipidemia and development of atherosclerosis and aneurysm in multiple mouse models. In further studies, we will identify HB-EGF signaling pathways for VLDL production in the liver. We employ liver-specific HB-EGF knockout liver cell system and in vitro liver cell line for this study.


Ongoing Research Support:

NIH-NHLBI K99/R00 HL105577 (Sangderk Lee, PI) 08/2011-07/2016
- Role of metalloproteinase-mediated EGFR signaling as a regulator of inflammatory responses to oxidized phospholipids in the vascular endothelium.

NIH-NIGM PILOT project, P20 GM103527 (Lisa Cassis, PI) 03/2016-02/2017
- Role of heparin binidng EGF-like growth factor (HB-EGF) in the development hyperlipidemia.
- Role: Co-Investigator

PubMed Publications: