Dr. Rus

Horea Rus, M.D.

Dr. Rus is an Professor with the Department of Neurology at the University of Maryland Medical School. He sees patients one day a week as well as runs a research laboratory. Dr. Rus is funded by the National Institute of Health, Veterans Administration and the National Multiple Sclerosis Society.

Dr. Rus's specific laboratory research lies in understanding the mechanisms of oligodendrocyte cell death through a process called apoptosis. Oligodendorcytes are special cells in the brain that make myelin. Myelin is wrapped around nerve fibers and helps increase the speed of nerve transmission. It is felt that injury or death of oligodendrocytes contributes to the MS disease process. In MS there are periods of time when the disease is most active. The hallmark of active MS is inflammation. During the active, inflammatory phase of multiple sclerosis, oligodendrocytes undergo apoptosis (or cell death). There are less oligodendrocytes therefore less ability to make myelin. This can contribute to the demyelinating process and the accumulation of disability.

In Dr. Rus's lab, he and his colleagues have shown that proteins once thought to only contribute to the destructive process in MS also may contribute to the prevention of oligodendrocyte death. Dr. Rus and his colleagues recently discovered a new protein (RGC-32) involved in activation of cell cycle in oligodendrocytes. They are now searching for ways to find if targeting of this protein might represent a potential treatment for MS. For more information on Dr. Rus's lab please go to: http://www.hruslab.com.

Dr. Rus sees patients in the Neurology Ambulatory Center on Monday afternoons. To make an appointment please call 410-328-4323.

Administrative Office Address: Patient Appointment Address:
Maryland Center for MS
110 South Paca St., 3rd floor
Baltimore, MD 21201
Phone 410-328-5605
Fax 410-328-5425
Neurology Ambulatory Center
16 South Eutaw Street, 3rd floor
Baltimore, MD 21201
Phone 410-328-4323
Fax 410-328-1149

Education and Training:
1980     M.D.

University of Medicine and Pharmacy
Cluj-Napoca, Romania
1992     Ph.D.

Immunology University of Medicine and Pharmacy
Cluj-Napoca, Romania

Internal Medicine,
Medical Clinic nr. 1
Cluj-Napoca, Romania

Clinical Pathology and Immunology
Cantacuzino Institute Bucharest, Romania

1999-2002 Resident in Neurology,
University of Maryland School of Medicine,
Department of Neurology,
Baltimore, MD

2002-2003 Fellow, Neuroimmunology,
University of Maryland School of Medicine,
Department of Neurology
Baltimore, MD
Licensed in Maryland- US
Current Appointments
2007- present Associate Professor of Neurology
University of Maryland School of Medicine

Selected publications and invited reviews (out of 110 published papers)

  • Badea, T., Niculescu, F., Shin, M.L., and Rus, H. Molecular cloning and characterization of RGC-32, a novel gene induced by complement activation in oligodendrocytes. J. Biol. Chem. 273, 26977-26981, 1998.
  • Soane, L., Rus, H., Niculescu, F., and Shin, M.L.: Inhibition of oligodendrocyte apoptosis by C5b-9 is associated with enhanced synthesis of Bcl-2 and mediated by inhibition of caspase-3 activation. J. Immunol. 163:6132-6138, 1999.
  • Rus, H., Niculescu, F., and Shin, M.L.: Role of the C5b-9 complement complex in cell cycle and apoptosis. Immunol. Rev.180: 49-55, 2001 (invited review).
  • Soane, L., Cho, H.J., Niculescu, F., Rus, H, and Shin, M.L.: C5b-9 terminal complement complex protects oligodendrocyte from death by regulating BAD through PI-3 kinase/Akt pathway. J. Immunol. 167: 2305-2311, 2001.
  • Rus, H. and Niculescu, F., Role of complement system in central nervous systems disease. Immunol. Res. 24, 79-86, 2001 (invited review).
  • Weerth S., Rus, H., Shin, M.L, and Raine, C.S.: Complement C5 in experimental autoimmune encephalomyelitis facilitates remyelination and prevents gliosis. Am. J. Pathol. 2003, 163, 1069-1080.
  • Niculescu T., Weerth, S., Niculescu F., Cudric, C.,Rus, V., Raine, CS., Shin, M.L.and Rus, H. Effectof complement C5 on apoptosis in experimental autoimmune encephalomyelitis. J. Immunol. 2004, 172, 5702-5707.
  • Rus H, Pardo CA, Hu L, Darrah E, Cudrici C, Niculescu T, Niculescu F, Mullen KM, Allie R, Guo L,Wulff H, Beeton C, Judge SI, Kerr DA, Knaus HG, Chandy KG, Calabresi PA. The voltage-gated potassium channel Kv1.3 is highly expressed on inflammatory infiltrates in multiple sclerosis brain. Proc Natl Acad Sci U S A. 2005;102:11094-9.
  • Cudrici C, Niculescu F, Jansen T, Zafranskaia K, Fosbrink M, Rus, V, Shin, ML, and Rus H. C5b-9 Terminal Complex Protects Oligodendrocytes from Apoptotic Cell Death by Inhibiting Caspase-8 Processing and Up-Regulating FLIP. J. Immunol. 2006; 176: 3173 – 3180.
  • Fosbrink, M, Niculescu, F, Rus V, Shin ML, Rus, H. C5b-9-induced endothelial cell proliferation and migration are dependent on Akt inactivation of forkhead transcription factor FOXO1. J Biol Chem. 2006, 281:19009-18.
  • Rus, H., Cudrici, C, David, S., Niculescu, F., The complement system in central nervous system diseases. Autoimmunity, 2006, 39, 395-402 (invited review).
  • Rus, H, Cudrici, C, Niculescu, F, Shin, M.L. Complement system in autoimmune demyelination: Dual role in neuroinflammation and neuroprotection. J. Neuroimmunol. 2006, 180, 9-16 (invited review).
  • Cudrici, C, Ito, T, Zafranskaia, E, Niculescu, F, Mullen, K, M, Vlaicu, S, Judge, S, Calabresi P. A, Rus, H. Dendritic cells are abundant in non-lesional gray matter in multiple sclerosis. Exp. Mol. Pathol. 2007, 83, 198-206.
  • Oh S, Cudrici, C, Ito, T, Rus, H. B-cells and humoral immunity in multiple sclerosis. Implications for therapy. Immunol Res. 2008, 40: 224-234
  • Cudrici, C, T. Ito, E. Zafranskaia, S. Weerth, H.H. Chen, A. Gherman, Niculescu, F, K. Soloviova, C. Tegla, V. Rus, C. S. Raine, Rus, H. Complement C5 regulates expression of Insulin-like growth factors binding proteins in chronic experimental allergic encephalomyelitis. J. Neuroimmunol. 2008 203, 94-103.
  • Fosbrink, M, Cudrici, C, Tegla, C. A., Soloviova, K, Ito, T, Vlaicu, S, Rus, V, Niculescu, F, Rus, H. Response gene to complement 32 is required for C5b-9 induced cell cycle activation in endothelial cells, Exp. Mol. Pathol. 2009, 86:87-94.
  • Tegla, CA, Cudrici, C, Rus, V, Ito, T, Vlaicu, S, Singh A, Rus, H. Neuroprotective effects of the complement terminal pathway during demyelination: Implications for oligodendrocyte survival. J. Neuroimmunol. 2009, 213, 3-11 (invited review).
  • Vlaicu, S., Tegla, TA, Cudrici, C, Fosbrink, M, Nguyen, V., Azimzadeh, P, Rus, V., Chen, H, Mircea, P, Rus, H. Epigenetic modifications induced by RGC-32 in colon cancer. Exp. Mol. Pathol. 2010, 88:67-76.
  • Ford C, Johnson K, Kachuck N, Linsey WJ, Lisak, R, Luzzio C, Myers, L, Panitch, H, Preiningerova, J, Pruitt, A, Rose, J, Rus, H., Wolinsky, J. Continuous long-term immunomodulatory therapy in relapsing-remitting multiple sclerosis: results from 15-year analysis of US prospective open-label study of glatiramer acetate. Mult Scler. 2010, 16, 342-350.
  • Tegla CA, Cudrici C, Rozycka M, Soloviova K, Ito T, Singh AK, Khan A, Azimzadeh P, Andrian-Albescu M, Khan A, Niculescu F, Rus V, Judge SI, Rus H. C5b-9-activated, K(v)1.3 channels mediate oligodendrocyte cell cycle activation and dedifferentiation. Exp Mol Pathol. 2011, 91:335-345.

For more information about the Maryland Center for Multiple Sclerosis, please call 410-328-5605.