"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 Professor 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.
Our research is focused on understanding how cholesterol changes immune cell function in the artery wall to contribute to chronic disease, such as atherosclerosis. We are particularly interested in how immune cell function is changed in patients with diabetes, as type 1 and type 2 diabetes sufferers are four times more likely to die of a heart attack than the general population.
There are two main aspects to our research. One is studying how the cholesterol content of immune cells, such as T cells and monocytes, changes the phenotype and function of these cells to modulate atherosclerosis development. Two proteins that we are particularly interested in are the ATP-binding cassette transporters ABCG1 and ABCA7. ABCG1 and ABCA7 are involved in the removal of excess cholesterol and phospholipid from cells; thus, they regulate the lipid content of cells. Using mice with targeted alterations of ABCG1 and ABCA7, we can study how T cell and monocyte function is disturbed by cholesterol and how this impacts disease. The second aspect of our research is to study the function of the NR4A family of nuclear receptors in atherosclerosis and other inflammatory diseases. We have recently discovered that one family member, NR4A1, is critically important for the development of a subset of monocytes in the bone marrow. We are exploring how NR4A1 regulates monocyte development, and how this nuclear receptor functions to regulate inflammation.
NR4A1 deletion polarizes macrophages toward an inflammatory phenotype and increases atherosclerosis. Circ Res. 2011
Monocyte and macrophage dynamics during atherogenesis. Arterioscler. Thromb Vasc Biol. 2011
The transcription factor NR4A1 controls bone marrow differentiation and survival of Ly6C- monocytes. Nat Immunol. 2011
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. 2010
Murine 12/15-lipoxygenase regulates ATP-binding cassette transporter G1 protein degradation through p38- and JNK2-dependent pathways. J Biol Chem. 2009
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