Darryl Peterson, PHD
In this section
Dr. Peterson received a Bachelor of Science degree in Biology from Wheaton College (IL), a Master of Arts degree in Zoology from Southern Illinois University, and a Doctor of Philosophy degree in Physiology from the University of Illinois Medical Center, Chicago. He did a post-doctoral fellowship in the Pathology Department at Northwestern University Medical School, under the mentorship of Dr. Frank A. Carone. He has held faculty positions at Northwestern University Medical School, The University of Illinois College of Medicine at Peoria, and the Chicago Medical School, where he is currently Professor of Physiology and Biophysics. Dr. Peterson has served as Acting Chairman of the Department of Physiology and Biophysics (Chicago Medical School), the President of the Academic Assembly (Chicago Medical School), and the Principal Senator of the University Senate (Rosalind Franklin University of Medicine and Science/Chicago Medical School). He has trained 8 graduate students as Major Advisor, including 4 M.D./Ph.D. students. Dr. Peterson does research on: 1) the pathophysiology of diabetic nephropathy, and 2) treatment of cerebrovascular stroke (please see Research link). He has published approximately 70 peer-reviewed scientific papers, and currently holds 2 U.S. patents for the treatment of stroke. He has served on 2 NIH study sections focusing on neuroscience and the blood-brain barrier.
Peterson, D.R. and R.A. Hawkins. Transport studies using membrane vesicles. In: Blood-Brain Barrier: Biology and Protocols. Humana Press, Inc. Totowa. Pp, 233-247, 2003.
Neuwelt, E.A., M.A. Pagel, D.F. Kraemer, D.R. Peterson, and L.L. Muldoon. Bone marrow chemoprotection without compromise of chemotherapy efficacy in rat brain tumor model. J. Pharmacol. Exp. Ther. 309: 1-6, 2004.
Doolittle, N.D., L.E. Abrey, W.A. Bleyer, S. Brem, T. Davis, P. Dorey-Duffy, L.R. Drewes, W.A. Hall, J.M. Hoffman, A.Korfel, R. Martuza, L.L. Muldoon, D. Peereboom, D.R. Peterson, S.D. Rabkin, Q. Smith, G. Stevens, and E.A. Neuwelt. New frontiers in translational research in neuro-oncology and the blood-brain barrier: report of the tenth annual blood-brain barrier disruption consortium meeting. Cancer Res. 11: 421-428, 2005.
Peterson, D.R. Blood-brain barrier. In: Encyclopedia of Life Sciences. Macmillan Reference Ltd., London, 2005.
Riser, B.L., S. Karoor, and D.R. Peterson. CCN genes and the kidney. In: CCN proteins: a new family of cell growth and differentiation regulators. B. Perbal and M. Takigawa, eds. Imperial College Press, UK, pp. 95-116, 2005.
Doolittle, N.D., D.M. Peereboom, G.A. Christoforidis, W.A. Hall, W.A., D. Palmieri, P.R. Brock, K. Campbell, D.T. Dickey, L.L. Muldoon, B.P. O’Neill, D.R. Peterson, B. Pollock, C. Soussain, Q. Smith, R.M. Tyson, and E.A. Neuwelt. Delivery of chemotherapy and antibodies across the blood-brain barrier and the role of chemoprotection in primary and metastatic brain tumors: report of the eleventh annual blood-brain barrier consortium meeting. J. Neuro-Oncology, 2006.
Cooker, L., D.R. Peterson, J. Rambow, M. Riser, R. Riser, F. Najmabadi, D. Brigstock, and B. Riser. TNF-alpha, but not IFN-gamma, regulates CCN2 (CTGF), collagen type I, and proliferation in mesangial cells: possible roles in the progression of renal fibrosis. Am. J. Physiol. F157-F165, 2007.
Dickey, D.T., L. L. Muldoon, N.D. Doolittle, D. R. Peterson, D.F. Kraemer, and E. A. Neuwelt. Effect of N-acetylcysteine route of administration on chemoprotection against cisplatin-induced nephrotoxicity in rat models. Cancer Chemother. Pharmacol. 62: 235-241, 2008.
Stenstrom, D.A., L.L. Muldoon, H. Armijo-Medina, S. Watnick, N. D. Doolittle, J. A. Kaufman, D.R. Peterson, J. Bubalo, and E.A. Neuwelt. Can N-acetylcysteine prevent contrast induced nephropathy: Premature phase III trials. J. Vasc. Interven. Radiol. 19: 309-318, 2008.
Riser, B.L., F. Najmabadi, B. Perbal, D.R. Peterson, J. Rambow, M.L. Riser. E. Sulowski, H. Yeger, and S.C. Riser. CCN3 (Nov) is a negative regulator of CCN2 (CTGF) and an endogenous inhibitor of the fibrotic pathway in an in vitro model of renal disease. Am. J. Pathol. 174: 1725-1734 2009.
Riser, B.L., F. Najmabadi, B. Perbal, , J. Rambow, M.L. Riser. E. Sukowski, H. Yeger, S.C. Riser, and D.R. Peterson. CCN3 (Nov): A negative regulator of CCN2 (CTGF) activity and an endogenous inhibitor of fibrosis in experimental diabetic nephropathy. In: CCN Proteins in Health and Disease. B. Perbal (ed.), pp. 163-181. Springer Science and Business Media, 2010.
Riser, B.L., F. Najmabadi, B. Perbal, J. Rambow, M.L. Riser, E. Sukowski, H. Yeger, S.C. Riser, and D.R. Peterson. CCN2/CCN3 regulation and the fibrosis of diabetic renal disease. J. Cell Comm. Signaling 4: 39-50, 2010.
Hawkins R.A., J.R. Viña, D.R. Peterson, R. O’Kane, A. Mokashi, and I. A. Simpson. Amino acid transport across each side of the blood-brain barrier. In: Amino Acids in Nutrition and Health. J.P.F. D’Mello, ed. CABI, pp. 191-214. CABI, Oxford, 2011.
Peterson, D.R. Blood-brain barrier. In: Encyclopedia of Life Sciences. Macmillan Reference Ltd., London, 2012.
Peterson, D.R. E.J. Sukowski, and D. Zikos. Blood-brain barrier transport pathways for cytoprotective thiols. Am J. Therapeutics, In press.
Blood-Brain Barrier Physiology, Pathophysiology of Stroke,
Renal Pathophysiology, Treatment for Diabetic Nephropathy
Current studies in our laboratory focus on: 1) functional properties of the blood-brain barrier, and prevention of injury to the blood-brain barrier associated with ischemic stroke; and 2) renal pathophysiology, and treatment and prevention of renal fibrosis associated with diabetic nephropathy.
The blood-brain barrier includes cerebral capillary endothelial cells that are sensitive to reperfusion injury associated with delayed thrombolysis following ischemic stroke. This can result in cerebral bleeding termed “hemorrhagic transformation”, culminating in death. We have been studying the cellular mechanisms responsible for blood-brain barrier injury and hemorrhagic transformation. Potential therapeutics for treatment of stroke, and protection of the cerebral vasculature under conditions of stroke, have been identified and tested.
Renal fibrosis associated with diabetes mellitus can contribute to chronic renal failure. We have been studying the cellular and molecular events responsible for renal fibrosis and diabetic nephropathy, including the design and development of drugs for treatment of these conditions.