Research Programs: Tumor Biology and Progression, Transplant Biology and Therapy
Regents Professor, Department of Medicine

hebbe001@umn.edu
612-624-6104 — office
612-626-4329 — lab
Preferred contact method: E-mail

Dr. Hebbel's clinical profile
(University of Minnesota Physicians Web site)

Robert P. Hebbel, M.D., holds the George Clark Professorship in the Department of Medicine and also is the Department's Vice-Chairman for Research. He received the MD degree from the University of Minnesota in 1973 and subsequently trained in Internal Medicine (at the University of Washington, Seattle) and hematology (at the University of Minnesota). Dr. Hebbel is a member of the Cancer Center, the Biomedical Engineering Institute, and the Lillehei Heart Institute.

Research Interests

Dr. Hebbel's research interests include: the vascular pathobiology of sickle disease; endothelial cell signal transduction and cell cycle in angiogenesis; genetic determination of endothelilal cell biology; and novel, endothelial-based gene therapy approaches to hemophilia and cancer.

Selected Publications

Belcher JD, Mahaseth H, Welch TE, Otterbein LE, Hebbel RP, Vercellotti GM.  Heme oxygenase-1 is a modulator of inflammation and vaso-occlusion in transgenic sickle mice.  J Clin Invest. 2006; 116:808-16.

De Meyer SF, Vanhoorelbeke K, Chuah MK, Pareyn I, Gillijns V, Hebbel RP, Collen D, Deckmyn H, Vandendriessche T.  Phenotypic correction of von Willebrand disease type 3 blood-derived endothelial cells with lentiviral vectors expressing von Willebrand factor.  Blood. 2006; 107:4728-36.

Stachelek SJ, Alferiev I, Connolly JM, Sacks M, Hebbel RP, Bianco R, Levy RJ. Cholesterol-modified polyurethane valve cusps demonstrate blood outgrowth endothelial cell adhesion post-seeding in vitro and in vivo.  Ann Thorac Surg. 2006; 81:47-55.

Wood KC, Hebbel RP, Granger DN.  Endothelial cell NADPH oxidase mediates the cerebral microvascular dysfunction in sickle cell transgenic mice.  FASEB J. 2005; 19:989-91.

Wood KC, Hebbel RP, Lefer DJ, Granger DN.  Critical role of endothelial cell-derived nitric oxide synthase in sickle cell disease-induced microvascular dysfunction.  Free Radic Biol Med. 2006; 40:1443-53.