biography
"My interest in diabetes began when I was a child, as my mother suffered from complications of type 1 diabetes, and so when I was little I always wanted to study it. Later, I became interested in type 2 diabetes as a global health concern. I hope my work at the La Jolla Institute will bring new opportunities to find therapies to reduce or prevent atherosclerosis development in patients with diabetes." - Catherine C. "Lynn" Hedrick, Ph.D.
Catherine C. "Lynn" Hedrick, PhD, is a Member in the Division of Inflammation Biology. Hedrick's lab is interested in sterol regulation immune function in atherosclerosis & diabetes.
Hedrick received her B.S. in Biology from Salem College in Winston-Salem, North Carolina in 1984. She received her Ph.D. in Biochemistry from Wake Forest University School of Medicine in 1992, where she performed her graduate research on LDL cholesterol metabolism in the laboratory of Dr Lawrence Rudel. From 1992 to 1995, she performed her postdoctoral research on HDL metabolism in the laboratory of Dr Aldons ‘Jake' Lusis at UCLA. From 1995 to 1999, she worked as a junior faculty member in the Division of Cardiology at UCLA, where her research focused on inflammation and endothelial function. From 2000 to 2009, Dr. Hedrick worked as a professor in the Departments of Pharmacology, Medicine, and Molecular Physiology and Biological Physics at the University of Virginia in Charlottesville. In 2009, Dr. Hedrick was awarded the Harrison Chair of Molecular Physiology and Biological Physics at the University of Virginia.
Dr. Hedrick currently serves on the NHLBI Program Project Grant Review Parent Committee, the NHLBI/NIDDK Animal Models of Diabetic Complications Committee, and the American Heart Association ATVB Council Leadership Committee. She is also a Fellow of the American Heart Association. Past honors received by Dr. Hedrick include the Atorvastatin National Award for Cardiovascular Research in 2000 and American Heart Association Young Investigator Awards in 1993 and 1995.
research focus
Lynn Hedrick, Ph.D. and her team study mechanisms in the artery wall that cause early atherosclerosis in patients with type 1 and type 2 diabetes. Type 1 and type 2 diabetes sufferers are four times more likely to die of a heart attack than the general population, leading Hedrick to believe that the diabetic environment in the body accelerates the likelihood that these disease patients will suffer heart attacks. In particular, Hedrick studies how elevated lipids, such as cholesterol, change immune cell function in diabetes to accelerate atherosclerosis development.
Hedrick's work has zeroed in on a protein called ABCG1, which acts as a cholesterol transporter. ABCG1 transfers excess cholesterol from cells to HDL for transport to the liver for elimination from the body. In 2008, Hedrick and her laboratory colleagues discovered that macrophages from patients with Type 2 diabetes had low levels of ABCG1, which led to cholesterol accumulation in the macrophages. Hedrick believes that low levels of ABCG1 contribute to lipid accumulation in macrophages, and may be a major cause of accelerated atherosclerosis development in patients with diabetes. Recently, Dr. Hedrick's group has discovered that ABCG1 regulates insulin secretion from beta cells in the pancreas, further suggesting a strong link between ABCG1 and diabetes. Hedrick's lab is focused on studying how ABCG1 expression is regulated in diabetes and the discovery of potential therapies that could reduce or prevent the development of atherosclerosis in these patients.
selected publications
An intracellular role for ABCG1-mediated cholesterol transport in the regulated secretory pathway of pancreatic beta cells. J Clin Invest. 2010
ABCG1 deficiency in mice promotes endothelial activation and monocyte-endothelial interactions. Arterioscler Thromb Vasc Biol. 2010
ATP-binding cassette transporter G1 (ABCG1) negatively regulates thymocyte and peripheral lymphocyte proliferation. J Immunol. 2009.
Murine 12/15-lipoxygenase regulates ATP-binding cassette transporter G1 protein degradation through p38- and JNK2-dependent pathways. J Biol Chem. 2009
G2A deficiency in mice promotes macrophage activation and atherosclerosis. Circ Res. 2009
Sphingosine-1-phosphate inhibits high glucose-mediated ERK1/2 action in endothelium through induction of MAP kinase phosphatase-3. Am J Physiol Cell Physiol. 2009
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