D. Neil Granger, Ph.D.
Boyd Professor and Head
Ph.D., 1977, University of Mississippi
Department of Molecular and Cellular Physiology
LSU Health Sciences Center
1501 Kings Highway
Shreveport, LA 71130
Neil Granger is Boyd Professor and Head of the Department of Molecular and Cellular Physiology. Born in Erath, LA, he attended the University of Southwestern Louisiana, earning the BS in microbiology in 1973. Granger received his doctorate in physiology and biophysics with Aubrey Taylor at the University of Mississippi Medical Center in 1977. He served on the faculty in the Department of Physiology at the University of South Alabama from 1977 to 1986 and then assumed his present position as department head at LSU Health Sciences Center, where he has also served at the Associate Dean for Research from 1993-2001. Granger is an author of over 600 articles in peer-review journals, over 100 book chapters and the author/editor of 6 books. He serves on the editorial boards of the Heart & Circulation, GI & Liver, and Cell sections of the American Journal of Physiology, as well as Circulation Research, Microcirculation, Shock, Pathophysiology, Free Radical Biology & Medicine, Lymphatic Research and Biology, Nitric Oxide Biology, and Experimental & Translational Stroke Medicine. He has also served on the editorial boards of NIPS, Gastroenterology, Digestive Diseases & Sciences, Journal of Critical Care, and Microvascular Research. Granger served as Associate Editor of the American Journal of Physiology: GI & Liver (1985-1991), Editor-in-Chief of Microcirculation (1999-2003), and Regional Editor for the Americas of Pathophysiology (2000-2007). He was a member of the Clinical Sciences-2 (1983-1986), Cardiovascular & Renal (1987-1991), General Medicine-A2 (1992-1996) and Gastrointestinal Mucosal Pathobiology Study Sections of the National Institutes of Health. He also served on several peer review panels and policy committees for the American Heart Association, the Research Committee of the American Gastroenterological Association, and the Physiology Test Committee of the National Board of Medical Examiners (1988-1991). Granger served on the Council of the Microcirculatory Society (1982-1985) and as its President in 1991-1992. He was elected to the Council of the American Physiological Society (APS, 1993-96) and served as its 77th President in 2004/5. He served on the Council of the Association of Chairs of Departments of Physiology (ACDP), and on the Board of Directors of the Federation of American Societies of Experimental Biology (FASEB). Granger has received several awards and honors for his research, including the APS Bowditch Award, the Distinguished Research Award from the GI Section of the APS, the Landis Award from the Microcirculatory Society, the Laerdal Award from the Society for Critical Care Medicine, the McKenna Memorial Award from the Canadian Association of Gastroenterology, the Dolph Adams Award from the Society for Leukocyte Biology, the Career of Distinction Award from the Oxygen Society, the Nishimaru-Tsuchiya International Award from the Japanese Society for Microcirculation, the Robert Berne Lecture & Award from the Cardiovascular Section of the APS, and the Zweifach Award & Lecture from the Microcirculatory Society. He was also designated as a Highly Cited Investigator (top 1 % of cited scientists) by the Institute for Scientific Information.
There are several established risk factors for the development of stroke, myocardial infarction and peripheral artery disease, including hypertension, hypercholesterolemia, obesity and diabetes. We are evaluating the influence of these risk factors on the microcirculation, under otherwise normal conditions and following ischemia and reperfusion. Our findings indicate that each of these risk factors lead to an exaggeration of the inflammatory responses and enhanced microvascular dysfunction following an ischemic insult. We also find that circulating blood cells, notably neutrophils, T-lymphocytes, and platelets, appear to contribute substantially to the deleterious responses to hypercholesterolemia and chronic arterial hypertension. We are attempting to define the chemical and molecular basis for the involvement and contribution of blood cells to the microvascular dysfunction that accompanies the presence of one or more risk factors for cardiovascular disease.
stroke, myocardial infarction
Intravital videomicroscopic measurements of leukocyte-endothelial cell adhesion · endothelial surface expression of adhesion molecules in regional vascular beds · in vivo measurements of oxidant stress, and endothelial barrier function · thrombus formation - genetically engineered animal models of human disease, including atherosclerosis, sickle cell disease, ischemic stroke, sepsis, and inflammatory bowel disease.
Janice Russell - Lab Manager