Dr. Sergiy Sukhanov obtained his MS in Biology in 1990 from Shevchenko Kiev State University (Ukraine) and his PhD in Molecular Biology/Virology in 1996 from Zabolotny Microbiology Institute (Ukraine). He trained as a postdoctoral fellow first at the Federal University of Sao Paulo (1998-1999, Sao Paulo, Brazil) and then at the Shevchenko Kiev State University (1999-2000) and the University of Missouri at Kansas City (2000-2002, Kansas City, MO). In 2002 he joined Cardiovascular Research Lab (PI: Dr. P. Delafontaine) in the University of Kansas-Medical Center (Kansas City, KS). In 2003 lab was moved to the Tulane University (New Orleans, LA) and Dr. Sukhanov was promoted to his first faculty position, as Research Assistant Professor in the Department of Medicine of the Tulane University Health Sciences Center. Dr.Sukhanov’s research focuses on studying mechanisms of atherosclerosis development using animal model and cultured cells such as vascular smooth muscle cells, endothelial cells and monocyte/macrophages. Dr.Sukhanov has published 18 papers in highly ranked scientific journals and has over 60 abstracts presented on international/domestic conferences. For his research contributions into area of cardiovascular diseases, Dr.Sukhanov received the Young Faculty Research Award from American Federation for Medical Research (twice, in 2008 and 2010) and he was awarded by Gordon Conference Scholarship Fund in 2009.
COBRE Research Summary:
Atherosclerosis is the principal underlying cause of most cardiovascular disease-related deaths, the leading cause of mortality in the USA. Insufficient energy production, impaired DNA repairing and smooth muscle cell (SMC) apoptosis are hallmarks of advanced atherosclerotic plaque. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a multifunctional glycolytic enzyme that plays a key role in energy production pathway and also GAPDH involves in maintenance the cell genome integrity and the cell apoptosis. We are the first to demonstrate the important link between the key pro-atherogenic molecule oxidized low-density lipoprotein (OxLDL), oxidative stress, GAPDH downregulation and inhibition of SMC energy metabolism. We also demonstrated an association between increased oxidative stress and reduced GAPDH levels within atherosclerotic plaque in vivo. The major hypothesis of COBRE project that restoring GAPDH levels in SMC would be protective against oxidant-induced apoptosis, impaired DNA repairing and suppression of cell migration in vitro and against diet-induced atherosclerosis in vivo. We plan to study whether an increase in GAPDH levels in aortic SMC reduces OxLDL-induced apoptosis and prevents suppression of SMC migration and study whether an OxLDL triggers GAPDH-specific effect on DNA repairing system. Using animal model of atherosclerosis (ApoE-deficient mice), we plan to study whether SMC-specific GAPDH overexpression suppresses atherosclerosis in vivo.
A brief list of selected publications:
Higashi Y, Sukhanov S, Anwar A, Shai SY, Delafontaine P. Aging, atherosclerosis, and IGF-1. J Gerontol A Biol Sci Med Sci. 2012;67(6):626-39. Review.
Rezk BM, Yoshida T, Semprun-Prieto L, Higashi Y, Sukhanov S, Delafontaine P. Angiotensin II infusion induces marked diaphragmatic skeletal muscle atrophy. PLoS One. 2012;7(1):e30276.
Sukhanov S, Higashi Y, Shai SY, Blackstock C, Galvez S, Vaughn C, Titterington J, Delafontaine P. Differential requirement for nitric oxide in IGF-1-induced anti-apoptotic, anti-oxidant and anti-atherosclerotic effects. FEBS Lett. 201;585(19):3065-72.
Sukhanov S, Semprun-Prieto L, Yoshida T, Michael Tabony A, Higashi Y, Galvez S, Delafontaine P. Angiotensin II, oxidative stress and skeletal muscle wasting. Am J Med Sci. 2011;342(2):143-7. Review.
Shai SY, Sukhanov S, Higashi Y, Vaughn C, Rosen CJ, Delafontaine P. Low circulating insulin-like growth factor I increases atherosclerosis in ApoE-deficient mice. Am J Physiol Heart Circ Physiol. 2011;300(5):H1898-906.
Shai SY, Sukhanov S, Higashi Y, Vaughn C, Kelly J, Delafontaine P. Smooth muscle cell-specific insulin-like growth factor-1 overexpression in Apoe-/- mice does not alter atherosclerotic plaque burden but increases features of plaque stability. Arterioscler Thromb Vasc Biol. 2010;30(10):1916-24.