H Rus

Summary

Affiliation: University of Maryland
Country: USA

Publications

  1. pmc Neuroprotective effects of the complement terminal pathway during demyelination: implications for oligodendrocyte survival
    Cosmin A Tegla
    Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    J Neuroimmunol 213:3-11. 2009
  2. ncbi request reprint The role of the complement system in innate immunity
    Horea Rus
    Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    Immunol Res 33:103-12. 2005
  3. ncbi request reprint C5b-9 complement complex in autoimmune demyelination and multiple sclerosis: dual role in neuroinflammation and neuroprotection
    Horea Rus
    University of Maryland at Baltimore, School of Medicine, Department of Neurology, 655 W Baltimore Street, BRB 12 016, Baltimore, MD 21201, USA
    Ann Med 37:97-104. 2005
  4. ncbi request reprint Role of the C5b-9 complement complex in cell cycle and apoptosis
    H G Rus
    University of Maryland School of Medicine, Department of Pathology, Baltimore, MD 21201, USA
    Immunol Rev 180:49-55. 2001
  5. ncbi request reprint The complement system in central nervous system diseases
    H Rus
    Department of Pathology, University of Maryland, School of Medicine, Baltimore 21201, USA
    Immunol Res 24:79-86. 2001
  6. ncbi request reprint Complement activation in autoimmune demyelination: dual role in neuroinflammation and neuroprotection
    Horea Rus
    Department of Neurology, Baltimore MD, USA
    J Neuroimmunol 180:9-16. 2006
  7. ncbi request reprint The complement system in central nervous system diseases
    Horea Rus
    Department of Neurology, School of Medicine, University of Maryland, Baltimore, MD 21201, USA
    Autoimmunity 39:395-402. 2006
  8. ncbi request reprint C5b-9 terminal complement complex protects oligodendrocytes from death by regulating Bad through phosphatidylinositol 3-kinase/Akt pathway
    L Soane
    Department of Pathology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    J Immunol 167:2305-11. 2001
  9. ncbi request reprint Tyrosine phosphorylation and activation of Janus kinase 1 and STAT3 by sublytic C5b-9 complement complex in aortic endothelial cells
    F Niculescu
    Department of Pathology, University of Maryland School of Medicine, Baltimore 21201, USA
    Immunopharmacology 42:187-93. 1999
  10. ncbi request reprint C5b-9 complement complex in autoimmune demyelination: dual role in neuroinflammation and neuroprotection
    Horea Rus
    Department of Neurology, University of Maryland, School of Medicine, Baltimore, MD 21201, USA
    Adv Exp Med Biol 586:139-51. 2006

Research Grants

  1. Regulation of Oligodendrocyte Survival
    Horea Rus; Fiscal Year: 2002
  2. Regulation of Oligodendrocyte Survival
    Horea Rus; Fiscal Year: 2003
  3. Regulation of Oligodendrocyte Survival
    Horea Rus; Fiscal Year: 2004
  4. Regulation of Oligodendrocyte Survival
    Horea Rus; Fiscal Year: 2005
  5. Regulation of Oligodendrocyte Survival
    Horea Rus; Fiscal Year: 2006

Collaborators

  • F Niculescu
  • P A Calabresi
  • S I Judge
  • Anthony Gaspari
  • Douglas Kerr
  • Carol Lee Koski
  • Cornelia Cudrici
  • Matthew Fosbrink
  • Violeta Rus
  • Moon L Shin
  • Teodora Niculescu
  • Takahiro Ito
  • William H Hoffman
  • Cosmin A Tegla
  • Sonia Vlaicu
  • Ekaterina Zafranskaia
  • Cynthia A Deboy
  • Sangjin Oh
  • Cornelia D Cudrici
  • Stefan David
  • L Soane
  • Cedric S Raine
  • Susanna Weerth
  • Lucian Soane
  • Tudor D Badea
  • Cosmin Tegla
  • Donald Small
  • Carlos A Pardo
  • Melina V Jones
  • Katharine A Whartenby
  • Kateryna Soloviova
  • M L Shin
  • Anil Singh
  • Katherine M Mullen
  • Sukriti Nag
  • Michael J Oglesbee
  • Roopa Venugopalan
  • Manuel F Casanova
  • Ekaterina Zakranskaia
  • Timothy Jensen
  • Sorana Hila
  • T C Badea
  • Jae Hyun Park
  • H J Cho

Detail Information

Publications32

  1. pmc Neuroprotective effects of the complement terminal pathway during demyelination: implications for oligodendrocyte survival
    Cosmin A Tegla
    Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    J Neuroimmunol 213:3-11. 2009
    ..These findings indicate that the activation of complement and C5b-9 assembly can also have protective roles during demyelination...
  2. ncbi request reprint The role of the complement system in innate immunity
    Horea Rus
    Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    Immunol Res 33:103-12. 2005
    ..All these data suggest that complement activation constitutes a critical link between the innate and acquired immune responses...
  3. ncbi request reprint C5b-9 complement complex in autoimmune demyelination and multiple sclerosis: dual role in neuroinflammation and neuroprotection
    Horea Rus
    University of Maryland at Baltimore, School of Medicine, Department of Neurology, 655 W Baltimore Street, BRB 12 016, Baltimore, MD 21201, USA
    Ann Med 37:97-104. 2005
    ..These findings indicate that activation of complement C5b-9 plays a pro-inflammatory role in the acute phase of the disease, but may also be neuroprotective during the chronic phase of the disease...
  4. ncbi request reprint Role of the C5b-9 complement complex in cell cycle and apoptosis
    H G Rus
    University of Maryland School of Medicine, Department of Pathology, Baltimore, MD 21201, USA
    Immunol Rev 180:49-55. 2001
    ..These findings indicate that complement activation and membrane assembly of sublytic C5b-9 play an important role in inflammation by promoting cell proliferation and by rescuing apoptotic cells...
  5. ncbi request reprint The complement system in central nervous system diseases
    H Rus
    Department of Pathology, University of Maryland, School of Medicine, Baltimore 21201, USA
    Immunol Res 24:79-86. 2001
    ..These findings indicate that complement activation and membrane assembly of C5b-9 play an important role in pathogenesis of central nervous system (CNS) disorders...
  6. ncbi request reprint Complement activation in autoimmune demyelination: dual role in neuroinflammation and neuroprotection
    Horea Rus
    Department of Neurology, Baltimore MD, USA
    J Neuroimmunol 180:9-16. 2006
    ..Our findings indicate that activation of complement and C5b-9 assembly plays a pro-inflammatory role in the acute phase, but may also be neuroprotective...
  7. ncbi request reprint The complement system in central nervous system diseases
    Horea Rus
    Department of Neurology, School of Medicine, University of Maryland, Baltimore, MD 21201, USA
    Autoimmunity 39:395-402. 2006
    ..These findings strongly suggest that complement activation and membrane assembly of C5b-9 can play a role in injury but can also provide neuroprotection depending on the pathophysiological context...
  8. ncbi request reprint C5b-9 terminal complement complex protects oligodendrocytes from death by regulating Bad through phosphatidylinositol 3-kinase/Akt pathway
    L Soane
    Department of Pathology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    J Immunol 167:2305-11. 2001
    ..This mechanism may be involved in the promotion of oligodendrocyte survival in inflammatory demyelinating disorders affecting the CNS...
  9. ncbi request reprint Tyrosine phosphorylation and activation of Janus kinase 1 and STAT3 by sublytic C5b-9 complement complex in aortic endothelial cells
    F Niculescu
    Department of Pathology, University of Maryland School of Medicine, Baltimore 21201, USA
    Immunopharmacology 42:187-93. 1999
    ..This study demonstrates the ability of membrane-inserted C5b-9 to activate JAK1 and STAT3 proteins, thus defining new signalling pathway by which C5b-9 may regulate gene activation...
  10. ncbi request reprint C5b-9 complement complex in autoimmune demyelination: dual role in neuroinflammation and neuroprotection
    Horea Rus
    Department of Neurology, University of Maryland, School of Medicine, Baltimore, MD 21201, USA
    Adv Exp Med Biol 586:139-51. 2006
  11. ncbi request reprint Molecular cloning and characterization of RGC-32, a novel gene induced by complement activation in oligodendrocytes
    T C Badea
    Department of Pathology, University of Maryland, School of Medicine, Baltimore, Maryland 21201, USA
    J Biol Chem 273:26977-81. 1998
    ..Overexpression of RGC-32 increased DNA synthesis in OLGxC6 glioma cell hybrids. These results suggest that RGC-32 may play a role in cell cycle activation...
  12. ncbi request reprint Complement activation and atherosclerosis
    F Niculescu
    Department of Pathology, University of Maryland, School of Medicine, Baltimore 21201, USA
    Mol Immunol 36:949-55. 1999
    ..Complement system activation is a major component of the chronic inflammatory process associated with atherosclerosis...
  13. ncbi request reprint Mechanisms of signal transduction activated by sublytic assembly of terminal complement complexes on nucleated cells
    F Niculescu
    University of Maryland, School of Medicine, Baltimore 21201, USA
    Immunol Res 24:191-9. 2001
    ..The key role of this signaling pathway is reflected on cell survival and proliferation in acute and chronic inflammation where complement activation is an ubiquitous event...
  14. ncbi request reprint Oligodendrocyte cell death in pathogenesis of multiple sclerosis: Protection of oligodendrocytes from apoptosis by complement
    Cornelia Cudrici
    Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    J Rehabil Res Dev 43:123-32. 2006
    ..These findings indicate that activated complement C5b-9 plays a proinflammatory role in acute MS but may also protect OLGs from death in chronic MS...
  15. ncbi request reprint Effects of complement C5 on apoptosis in experimental autoimmune encephalomyelitis
    Teodora Niculescu
    Department of Pathology, University of Maryland, School of Medicine, Baltimore, MD 21201, USA
    J Immunol 172:5702-6. 2004
    ..Together, these findings are consistent with the role of C5, possibly by forming the membrane attack complex, in limiting OLG apoptosis in EAE, thus promoting remyelination during recovery...
  16. ncbi request reprint B-cells and humoral immunity in multiple sclerosis. Implications for therapy
    Sangjin Oh
    Department of Neurology, School of Medicine, University of Maryland, Baltimore, MD 21201, USA
    Immunol Res 40:224-34. 2008
    ..Thus, the role played by B-cells and humoral immunity is rather complex, and new strategies for targeting B-cell responses are continuing to emerge...
  17. ncbi request reprint C5b-9 terminal complex protects oligodendrocytes from apoptotic cell death by inhibiting caspase-8 processing and up-regulating FLIP
    Cornelia Cudrici
    Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    J Immunol 176:3173-80. 2006
    ..C5b-9 also down-regulated the expression of FasL and the Fas-induced apoptosis. These data suggest that C5b-9 through PI3K signaling can rescue OLG from Fas-mediated apoptosis by regulating caspase-8 processing...
  18. pmc Dendritic cells are abundant in non-lesional gray matter in multiple sclerosis
    Cornelia Cudrici
    Department of Neurology, University of Maryland, Baltimore, MD 21201, USA
    Exp Mol Pathol 83:198-206. 2007
    ..Since injury to the NLGM is one of the key factors associated with disability accumulation, targeting DCs may represent a possible new therapeutic approach in MS to prevent disease progression...
  19. pmc The voltage-gated potassium channel Kv1.3 is highly expressed on inflammatory infiltrates in multiple sclerosis brain
    Horea Rus
    Department of Neurology, The Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, MD 21287, USA
    Proc Natl Acad Sci U S A 102:11094-9. 2005
    ..3(high)/CCR7(-) T(EM), suggesting that a subset of cerebrospinal fluid cells existed in a primed state ready to become T(EM). These studies provide further rationale for the use of specific Kv1.3 antagonists in MS...
  20. pmc Response gene to complement 32 is required for C5b-9 induced cell cycle activation in endothelial cells
    Matthew Fosbrink
    Department of Neurology, University of Maryland, School of Medicine, Baltimore, MD 21201, USA
    Exp Mol Pathol 86:87-94. 2009
    ..All these data together suggest that cell cycle induction by C5b-9 in AEC is RGC-32 dependent and this is in part through regulation of Akt and growth factor release...
  21. ncbi request reprint Sublytic terminal complement attack induces c-fos transcriptional activation in myotubes
    Tudor D Badea
    Department of Pathology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    J Neuroimmunol 142:58-66. 2003
    ..We propose that c-fos gene transcription associated with myotube dedifferentiation is induced by C5b-9 through ERK1-mediated assembly of serum response factor-ternary complex...
  22. ncbi request reprint C5b-9 terminal complement complex assembly on apoptotic cells in human arterial wall with atherosclerosis
    Florin Niculescu
    Department of Pathology, School of Medicine, University of Maryland, Baltimore, MD 21201, USA
    Exp Mol Pathol 76:17-23. 2004
    ..In conclusion, some apoptotic cells carry C5b-9 deposits, suggesting that complement might be activated by apoptotic cells and involved in the promotion of apoptosis, contributing to the progression of atherosclerotic lesions...
  23. ncbi request reprint Effects of membrane attack complex of complement on apoptosis in experimental autoimmune encephalomyelitis
    Teodora Niculescu
    University of Maryland, School of Medicine, Baltimore, Maryland 21201, USA
    Ann N Y Acad Sci 1010:530-3. 2003
    ..These results indicate that C5 and possibly MAC may be required for the limitation of inflammatory response within the central nervous system...
  24. ncbi request reprint The role of c5b-9 terminal complement complex in activation of the cell cycle and transcription
    Matthew Fosbrink
    Toxicology Program, University of Maryland, Baltimore, MD 21201, USA
    Immunol Res 31:37-46. 2005
    ..RGC-32 may play a key role in cell-cycle activation by increasing cyclin B1-CDC2 activity. C5b-9-mediated cell-cycle activation plays an important role in cellular proliferation and protection from apoptosis...
  25. ncbi request reprint Both apoptosis and complement membrane attack complex deposition are major features of murine acute graft-vs.-host disease
    Florin Niculescu
    Department of Medicine, Division of Rheumatology and Clinical Immunology, Baltimore, MD 21201, USA
    Exp Mol Pathol 79:136-45. 2005
    ..These results indicate a role for both adaptive immunity and innate immunity in this model of GVHD and support its use in modeling human acute GVHD in the nonmyeloablative setting...
  26. ncbi request reprint C5b-9-induced endothelial cell proliferation and migration are dependent on Akt inactivation of forkhead transcription factor FOXO1
    Matthew Fosbrink
    Department of Neurology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    J Biol Chem 281:19009-18. 2006
    ..Our data indicate that C5b-9 regulation of the cell cycle activation in AEC through Akt pathway is dependent on inactivation of FOXO1...
  27. ncbi request reprint JNK1 activation mediates C5b-9-induced P0 mRNA instability and P0 gene expression in Schwann cells
    Stefan David
    Department of Neurology, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    J Peripher Nerv Syst 11:77-87. 2006
    ..Our results indicate that the ability of C5b-9 in vitro to affect P0 gene expression is mediated via JNK1 activation that leads to enhanced mRNA decay and transcriptional repression of P0...
  28. pmc FLT-3 expression and function on microglia in multiple sclerosis
    Cynthia A Deboy
    Neurology, Johns Hopkins University, Pathology 627, 600 N Wolfe Street, Baltimore, MD 21287, USA
    Exp Mol Pathol 89:109-16. 2010
    ..Furthermore these data suggest that FLT-3 may be a therapeutic target on microglia to mitigate CNS inflammation...
  29. ncbi request reprint Complement activation in diabetic ketoacidosis brains
    William H Hoffman
    Department of Pediatrics, Medical College of Georgia, Augusta, GA 30912, USA
    Exp Mol Pathol 80:283-8. 2006
    ....
  30. ncbi request reprint The role of complement activation in atherosclerosis
    Florin Niculescu
    Department of Pathology University of Maryland School of Medicine Baltimore, MD 21201 USA
    Immunol Res 30:73-80. 2004
    ..All these data suggest that activation of the complement system plays an important role in atherogenesis...
  31. pmc Neuroinflammatory response of the choroid plexus epithelium in fatal diabetic ketoacidosis
    William H Hoffman
    Department of Pediatrics, Medical College of Georgia, Augusta, GA 30912, USA
    Exp Mol Pathol 83:65-72. 2007
    ..Our data demonstrate the presence of a multifaceted neuroinflammatory cytotoxic insult of the CPE, which may play a role in the pathophysiology of the fatal brain edema of DKA...
  32. ncbi request reprint Association of complement inhibitors with connective tissue matrix in atherosclerotic lesions
    Horea Rus
    Arterioscler Thromb Vasc Biol 23:1478. 2003

Research Grants5

  1. Regulation of Oligodendrocyte Survival
    Horea Rus; Fiscal Year: 2002
    ..Our proposed studies will provide an unique model system to elucidate the biology of sublethally injured OLG and may lead to the identification of regulatory factors that can enhance OLG survival and remyelination. ..
  2. Regulation of Oligodendrocyte Survival
    Horea Rus; Fiscal Year: 2003
    ..Our proposed studies will provide an unique model system to elucidate the biology of sublethally injured OLG and may lead to the identification of regulatory factors that can enhance OLG survival and remyelination. ..
  3. Regulation of Oligodendrocyte Survival
    Horea Rus; Fiscal Year: 2004
    ..Our proposed studies will provide an unique model system to elucidate the biology of sublethally injured OLG and may lead to the identification of regulatory factors that can enhance OLG survival and remyelination. ..
  4. Regulation of Oligodendrocyte Survival
    Horea Rus; Fiscal Year: 2005
    ..Our proposed studies will provide an unique model system to elucidate the biology of sublethally injured OLG and may lead to the identification of regulatory factors that can enhance OLG survival and remyelination. ..
  5. Regulation of Oligodendrocyte Survival
    Horea Rus; Fiscal Year: 2006
    ..Our proposed studies will provide an unique model system to elucidate the biology of sublethally injured OLG and may lead to the identification of regulatory factors that can enhance OLG survival and remyelination. ..