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Pathobiology Research


Lysophosphatidic Acid and Tissue Factor in Atherosclerosis

Mei-Zhen Cui
Ph.D., Tokyo Institute of Technology, Japan
Associate Professor
Faculty Web Page


Atherosclerosis accounts for nearly 75% of deaths from cardiovascular disease. The buildup of plaque (fatty deposits and other cellular debris) on the arterial walls can erode the wall of the artery, reduce elasticity, and impede blood flow. Plaques that rupture cause thrombosis (the formation of a clot inside a blood vessel) which can obstruct blood flow and lead to myocardial infarction, stroke, and sudden death.

Tissue factor (TF), a transmembrane glycoprotein, is the principal initiator of the coagulation cascade, a complex chain reaction that converts prothrombin to thrombin, which catalyzes the eventual formation of a clot. Thrombin induces the proliferation of smooth muscle cells; TF induces smooth muscle cell migration. Migration of smooth muscle cells from the medial to the intimal layer of the arterial wall and the subsequent proliferation of these cells plays a critical role in the pathogenesis of atherosclerosis.

TF expressed on the vascular smooth muscle cell surface is pathologically significant as a contributor to plaque growth, thrombus formation, and acute coronary syndrome following plaque rupture. However, the mechanisms that regulate TF gene expression and the regulatory signaling pathways in smooth muscle cells are largely unknown.

Oxidized low-density lipoprotein (oxLDL) has many atherogenic properties, but the mechanisms involved are not well understood. Research indicates that oxidized low-density lipoprotein may contribute to the pathogenesis of atherosclerosis by up-regulating TF expression.

Dr. Cui has made remarkable progress towards understanding the regulatory effects of oxLDL on TF expression. Recently, Dr. Cui’s group has reported that lysophosphatidic acid (LPA), a component of oxLDL, induces TF in mRNA, TF protein, and TF activity in vascular smooth muscle cells. Dr. Cui’s data also demonstrate that LPA-induced TF expression is controlled at the transcriptional level. Studies ongoing in Dr. Cui’s laboratory are directed towards understanding the cellular signaling pathways that mediate the biological effects of LPA, specifically the effects on gene expression.

Results from Dr. Cui’s studies could lead to the identification of new therapeutic targets for the prevention and treatment of atherosclerosis.


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