Henning Schroeder
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Henning Schroeder, Ph.D. Telephone Number: FAX Number: E-mail Address: |
Education:
Pharmacy Degree (“Pharmazeutische Prüfung”), Düsseldorf University, 1981
Ph.D. in Pharmacology, Düsseldorf University, 1985
Post-doctoral Fellowship in Cell Signaling, Stanford University, 1987
Positions and Employment:
| 1992 | Assistant Professor, (“Privatdozent”), Department of Pharmacology, Düsseldorf University School of Medicine, FRG |
| 1993 | Visiting Scholar, Division of Oncology, Stanford University School of Medicine, California |
| 1995 | Professor and Chair, Department of Pharmacology, Martin Luther University School of Pharmacy, Halle, FRG |
| 2005 | Visiting Professor, Division of Neonatology, Stanford University School of Medicine, California |
| 2007 | Associate Dean for Research and Graduate Studies, College of Pharmacy, University of Minnesota, Minneapolis |
| 2007 | Professor, Department of Pharmaceutics, College of Pharmacy, University of Minnesota, Minneapolis |
Honors and Awards:
| 1986 | DFG fellowship, Postdoctoral Fellow, Stanford University School of Medicine |
| 1991 | Edens Prize of the Heinrich Heine University Düsseldorf |
| 1991 | Prize of the "Therapiewoche Karlsruhe 1991" |
| 1992 | DFG fellowship, Visiting Scholar, Stanford University School of Medicine |
| 1994 | Heisenberg Fellowship (DFG) |
| 1997 | Innovation Prize of the Martin Luther University Halle Wittenberg |
| 1999 | Scientific Advisory Board of the International Society of Heart Failure |
| 2001 | Fellow of the American Heart Association (F.A.H.A.) |
| 2002 | Scientific Advisory Board, Federal Pharmacists Association, FRG |
| 2004 | Phoenix Pharmaceutical Sciences Award |
Research Interests:
Dr. Schroeder’s research focuses on the regulation of antioxidant proteins and their potential role as therapeutic targets in atherosclerosis. One of these candidate proteins is heme oxygenase-1 (HO-1) which degrades heme and generates bilirubin and carbon monoxide (CO). Both products have strong antioxidant and anti-inflammatory properties. CO, in addition, acts as a dilator of blood vessels. HO-1 has been shown to be a target and mediator of established drugs such as aspirin, the statins, and organic nitrates (nitric oxide donors). Recent data indicate that some bioactive peptides (e.g., derived from fish or soy) and other micronutrients function as inducers of HO-1 which may explain their antioxidant and antihypertensive properties.
Although a number of agents induce HO-1 via nitric oxide and cyclic nucleotides (cGMP / cAMP), Dr. Schroeder’s lab has demonstrated the existence of additional, as yet unexplored, pathways. His research team continues to characterize the various signaling routes and mediators involved in HO-1 expression and to study their relevance in the treatment of cardiovascular disease and other inflammatory processes such as ischemia and reperfusion injury, Alzheimers disease, transplant rejection, and autoimmume disorders (e.g., rheumatoid arthritis, psoriasis).
Functionally, increased expression of HO-1 leads to protection from oxidant injury in endothelial cells and to a reduction in renal toxicity of immunosuppressants such as cyclosporin A. Besides examining transcriptional and translational regulation, Dr. Schroeder’s group is also monitoring the changes in the formation of downstream products and mediators such as bilirubin and ferritin. The ultimate goals of these studies are to explore the underlying molecular mechanisms and, more importantly, to find clinical markers for the induction of antioxidant genes.
Selected publications:
Erdmann K, Cheung BWY, Schröder H. The possible role of food-derived bioactive peptides in reducing the risk of cardiovascular disease. J. Nutr. Biochem. May 19, 2008 [Epub ahead of print].
Erdmann K, Grosser N, Schipporeit K and Schröder H. The ACE inhibitory dipeptide Met-Tyr diminishes free radical formation in human endothelial cells via induction of heme oxygenase-1 and ferritin. J. Nutr. 136: 1-5 (2006).
Schröder H. No nitric oxide for HO-1 from sodium nitroprusside. Mol. Pharmacol. 69: 1507-1509 (2006).
Schröder H. Novel pathways for an old drug: lipoxin A4 may mediate heme oxygenase-1 induction by aspirin. Am. J. Physiol. Cell. Physiol. 289: C507-C508 (2005).
Schmidt P, Schramm M, Schröder H, Wunder F and Stasch J-P. Identification of residues crucially involved in the binding of the heme moiety of soluble guanylate cyclase. J. Biol. Chem. 279: 3025-3032 (2004).
Grosser N, Hemmerle A, Berndt G, Erdmann K, Hinkelmann U, Schürger S, Wijayanti N, Immenschuh S and Schröder H. The antioxidant defense protein heme oxygenase-1 is a novel target for statins in endothelial cells. Free Radic. Biol. Med. 37: 2064-2071 (2004).
Stasch J-P, Becker EM, Alonso-Alija C, Apeler H, Dembowsky K, Feurer A, Gerzer R, Minuth T, Perzborn E, Pleiss U, Schröder H, Schroeder W, Stahl E, Steinke W, Straub A and Schramm M. NO-independent regulatory site on soluble guanylate cyclase and therapeutic implications. Nature 410: 212-215 (2001).
Polte T, Abate A, Dennery PA and Schröder H. Heme oxygenase-1 is a cyclic GMP-inducible endothelial protein and mediates the cytoprotective action of nitric oxide. Arterioscler. Thromb. Vasc. Biol. 20: 1209-1215 (2000).
Oberle S, Polte T, Abate A, Podhaisky H-P and Schröder H. Aspirin increases ferritin synthesis in endothelial cells: a novel antioxidant pathway. Circ. Res. 82: 1016-1020 (1998).
Schröder H, Leitman DC, Bennett BM, Waldman SA and Murad F. Glyceryl trinitrate-induced desensitization of guanylate cyclase in cultured rat lung fibroblasts. J. Pharmacol. Exp. Ther. 245: 413-418 (1988).
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