David W. Busija, Ph.D, Professor
Dr. Busija received his Ph.D. in 1978 from the University of Kansas and completed his post-doctoral training at the Cardiovascular Center at the University of Iowa. Following faculty positions at Johns Hopkins Medical School and the University of Tennessee Medical School in Memphis, he came to Wake Forest University Health Sciences in 1990 to join the Department of Physiology and Pharmacology. His laboratory has published over 250 papers on various aspects of vascular and brain physiology and pathology. He also has a record of success in training a diverse array of students, fellows, and younger faculty in his laboratory to be independent scientists.

SYNOPSIS OF AREA OF INTEREST: : Current studies address: 1) the effects of reactive oxygen species derived from the NAD(P)H oxidase system on the function of cerebral resistance arteries and brain in insulin resistant animals; 2) the molecular characterization of ATP-sensitive potassium channels in brain mitochondria and the role of these channels in protecting the brain against injury; 3) the molecular characterization of cyclooxygenase isoforms in vascular and neural tissues following injury; and 4) the physiology and pathology of the perinatal cerebral circulation.

DETAILED AREA OF INTEREST: Dr. Busija has a well established, diverse research program, focusing on the role of mitochondrial ATP-sensitive potassium channels in tissue and cellular protection, the regulation of expression of cyclooxygenase isoforms in vascular and brain cells, the pathophysiology of cerebral ischemia, and mechanisms of vascular dysfunction and increased neuronal injury related to insulin resistance. This program integrates traditional biochemical, pharmacological and physiological approaches in laboratory animals with up-to-date techniques in cell culture and molecular biology. In the last several years, Dr. Busija played a leadership role in several research areas and was the first investigator to target the mitochondrial KATP channels to protect the brain against ischemic and chemical challenges, the first to clone the rat and mouse COX-3 isoforms, and the first to examine effects of insulin resistance on the cerebral circulation and to define the role of NAD(P)H oxidase in resultant cerebral vascular dysfunction.

PUBLICATIONS:

Busija DW, Miller AW, Katakam P, Erdos B. Insulin resistance and associated dysfunction of resistance vessels and arterial hypertension. Minerva Medica 96:223-232, 2005.

Lenzser G, Kis B, Bari F, Busija DW. Diazoxide preconditioning attenuates global cerebral ischemia-induced blood-brain barrier permeability. Brain Res 105:72-80, 2005.

Busija DW, Katakam P, Rajapakse NC, Kis B, Grover G, Domoki F, Bari F. Effects of ATP-sensitive potassium channel activators diazoxide and BMS-191095 on membrane potential and reactive oxygen species production in isolated piglet mitochondria. Brain Res Bull 66:85-90, 2005.

Kis B, Snipes JA, Busija DW. Acetaminophen and the COX-3 puzzle: Sorting out Facts, Fictions, and Uncertainties. J Pharmacol Exp Ther 315:1-7, 2005.
Katakam P, Tulbert CD, Snipes JA, Erdos B, Miller AW, Busija DW. Impaired insulin-induced vasodilation in small coronary arteries of Zucker Obese rats is mediated by reactive oxygen species. Am J Physiol 288:H854-860, 2005.

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