Physician, Chief Renal Section -Joslin Diabetes Ce
Office:
Phone:
617-732-2477
Fax:
617-732-2467
Email:
rstanton@bidmc.harvard.edu
Address:
Beth Israel Deaconess Medical Center 330 Brookline Ave
Boston, MA 02215
Advanced Degree And Training Info:
Year
Institution
Area or Rank
1980
Hahnemann Medical College (Drexel University)
Medicine
1983
Oregon Health Sciences University
Chief Resident Instuctor
1984
Brigham and Women
Postdoctoral Fellow
1987
Brigham and Women
Instructor
1991
Joslin Diabetes Center Beth Israel Deaconess Medical Center and Harvard Med
Assistant Professor
1995
Joslin Diabetes Center
Chief Renal Section
2006
Joslin Diabetes Center Beth Israel Deaconess Medical Center and Harvard Med
Associate Professor
Research Team Listing
No team members listed
Areas of Interest:
Cancer & Hematologic
Cardiovascular
Metabolic / Metabolic Diseases
Vascular Biology
Major Research Theme:
Dr. Stanton has pioneered a new approach to the treatment and possible prevention of diabetic complications by discovering that a chemical of central importance to cell survival and many other cellular functions, called NADPH which is mainly produced by the enzyme glucose 6-phosphate dehydrogenase (G6PD), is abnormally regulated in cultured cells exposed to high glucose and in diabetic animals. Dr. Stanton's lab has previously shown that G6PD and NADPH play a central role in supporting normal cell growth and in preventing cell death. NADPH is absolutely required by many critical cellular systems such as the antioxidant system, nitric oxide production, and NADPH oxidase. Dr. Stanton's laboratory has shown that high glucose stimulates a deleterious series of events - decrease in NADPH level and redistribution of intracellular NADPH availability that results in decreased antioxidant cellular function, decreased nitric oxide production, and increased NADPH oxidase activity. These events lead to endothelial cell damage, scarring of blood vessels, and high blood pressure and ultimately to heart attacks, strokes, and kidney failure. Fixing the regulatory problems with G6PD and NADPH holds tremendous promise in preventing these endothelial cell problems and thus preventing diabetic complications.
Tian WN, Braunstein LD, Pang J, Stuhlmeier KM, Xi QC, Tian X, Stanton RC. Importance of glucose-6-phosphate dehydrogenase activity for cell growth. J Biol Chem. 1998;273(17):10609-10617.
Tian WN, Braunstein LD, Apse K, Pang J, Rose M, Tian X, Stanton RC. Importance of glucose-6-phosphate dehydrogenase activity in cell death. Am J Physiol. 1999;276(5 Pt 1):C1121-1131.
Zhang Z, Apse K, Pang J, Stanton RC. High glucose inhibits glucose-6-phosphate dehydrogenase via cAMP in aortic endothelial cells. J Biol Chem. 2000;275(51):40042-40047.
Xu Y, Osborne B, and Stanton RC. Diabetes causes inhibition of glucose-6-phosphate dehydrogenase via activation of protein kinase A which contributes to oxidative stress in rat kidney cortex. Am J Physiol. 2005;289:F1040-F1047.
Leopold JA Dam A, Scribner AW, Liao R, Diane E. Handy, DE, Stanton RC, Pitt B, and Loscalzo J. Aldosterone impairs vascular reactivity by decreasing glucose-6-phosphate dehydrogenase activity. Nature Medicine. 2007;13(2):189-197.
External Recognition:
Honorary Professorship, Southern Medical University, Guangzhou, China
Major Collaborative Activities:
Dr. Stanton maintains a very active, on-going collaboration with Joseph Loscalzo, MD (Chairman of the Department of Medicine, Brigham and Women's Hospital).
