S R Goldring

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Pathogenesis of bone erosions in rheumatoid arthritis
    S R Goldring
    Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA
    Curr Opin Rheumatol 12:195-9. 2000
  2. ncbi request reprint Inflammatory mediators as essential elements in bone remodeling
    S R Goldring
    Beth Israel Deaconess Medical Center, Harvard Medical School, New England Baptist Bone and Joint Institute Harvard Institutes of Medicine, Boston, MA, USA
    Calcif Tissue Int 73:97-100. 2003
  3. ncbi request reprint Pathogenesis of bone and cartilage destruction in rheumatoid arthritis
    S R Goldring
    Harvard Medical School, New England Baptist Bone and Joint Institute, Boston, MA, USA
    Rheumatology (Oxford) 42:ii11-6. 2003
  4. ncbi request reprint Bone and joint destruction in rheumatoid arthritis: what is really happening?
    Steven R Goldring
    Harvard Medical School, New England Baptist Bone and Joint Institute, Boston, Massachusetts 02215, USA
    J Rheumatol Suppl 65:44-8. 2002
  5. ncbi request reprint Pathogenesis of bone lesions in rheumatoid arthritis
    Steven R Goldring
    Harvard Institutes of Medicine, Room 241, 4 Blackfan Circle, Boston, MA 02115, USA
    Curr Rheumatol Rep 4:226-31. 2002
  6. ncbi request reprint Pathogenesis of bone erosions in rheumatoid arthritis
    Steven R Goldring
    Beth Israel Deaconess Medical Center, Harvard Medical School, and New England Baptist Bone and Joint Institute, Harvard Institutes of Medicine, Boston, Massachusetts 02115, USA
    Curr Opin Rheumatol 14:406-10. 2002
  7. doi request reprint The role of cell-substrate interaction in regulating osteoclast activation: potential implications in targeting bone loss in rheumatoid arthritis
    K P McHugh
    Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
    Ann Rheum Dis 69:i83-85. 2010
  8. pmc Angiopoietin-1 is expressed in the synovium of patients with rheumatoid arthritis and is induced by tumour necrosis factor alpha
    E M Gravallese
    Beth Israel Deaconess Medical Center, Department of Medicine, New England Baptist Bone and Joint Institute, Harvard Institutes of Medicine, 4 Blackfan Circle, Boston, MA 02115, USA
    Ann Rheum Dis 62:100-7. 2003
  9. ncbi request reprint Role of cell-matrix interactions in osteoclast differentiation
    K P McHugh
    Department of Orthopaedics and Rheumatology, Beth Israel Deaconess Medical Center, New England Baptist Hospital, and New England Baptist Bone and Joint Institute, Harvard Medical School, Boston, MA, USA
    Adv Exp Med Biol 602:107-11. 2007
  10. pmc The role of TNF-receptor family members and other TRAF-dependent receptors in bone resorption
    E M Gravallese
    Beth Israel Deaconess Medical Center, New England Baptist Bone and Joint Institute, Harvard Institutes of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Arthritis Res 3:6-12. 2001

Collaborators

Detail Information

Publications34

  1. ncbi request reprint Pathogenesis of bone erosions in rheumatoid arthritis
    S R Goldring
    Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA
    Curr Opin Rheumatol 12:195-9. 2000
    ..This paper reviews the cellular mechanisms and factors implicated in bone erosions in rheumatoid arthritis, and discusses the possible therapeutic strategies suggested by these findings...
  2. ncbi request reprint Inflammatory mediators as essential elements in bone remodeling
    S R Goldring
    Beth Israel Deaconess Medical Center, Harvard Medical School, New England Baptist Bone and Joint Institute Harvard Institutes of Medicine, Boston, MA, USA
    Calcif Tissue Int 73:97-100. 2003
    ..These observations have important implications with respect to the development of therapeutic strategies to prevent bone loss in inflammatory conditions...
  3. ncbi request reprint Pathogenesis of bone and cartilage destruction in rheumatoid arthritis
    S R Goldring
    Harvard Medical School, New England Baptist Bone and Joint Institute, Boston, MA, USA
    Rheumatology (Oxford) 42:ii11-6. 2003
    ....
  4. ncbi request reprint Bone and joint destruction in rheumatoid arthritis: what is really happening?
    Steven R Goldring
    Harvard Medical School, New England Baptist Bone and Joint Institute, Boston, Massachusetts 02215, USA
    J Rheumatol Suppl 65:44-8. 2002
    ..These observations suggest that osteoclasts mediate focal bone erosions in RA and that targeting of osteoclasts and osteoclast mediated bone resorption represents a rational approach to preventing or reducing focal bone loss in RA...
  5. ncbi request reprint Pathogenesis of bone lesions in rheumatoid arthritis
    Steven R Goldring
    Harvard Institutes of Medicine, Room 241, 4 Blackfan Circle, Boston, MA 02115, USA
    Curr Rheumatol Rep 4:226-31. 2002
    ....
  6. ncbi request reprint Pathogenesis of bone erosions in rheumatoid arthritis
    Steven R Goldring
    Beth Israel Deaconess Medical Center, Harvard Medical School, and New England Baptist Bone and Joint Institute, Harvard Institutes of Medicine, Boston, Massachusetts 02115, USA
    Curr Opin Rheumatol 14:406-10. 2002
    ..These findings provide a rational framework for developing targeted therapies that can specifically inhibit or slow the progressive focal bone destruction associated with the rheumatoid synovial lesion...
  7. doi request reprint The role of cell-substrate interaction in regulating osteoclast activation: potential implications in targeting bone loss in rheumatoid arthritis
    K P McHugh
    Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
    Ann Rheum Dis 69:i83-85. 2010
    ....
  8. pmc Angiopoietin-1 is expressed in the synovium of patients with rheumatoid arthritis and is induced by tumour necrosis factor alpha
    E M Gravallese
    Beth Israel Deaconess Medical Center, Department of Medicine, New England Baptist Bone and Joint Institute, Harvard Institutes of Medicine, 4 Blackfan Circle, Boston, MA 02115, USA
    Ann Rheum Dis 62:100-7. 2003
    ..To examine the potential role of the angiogenic growth factor angiopoietin-1 (Ang-1) in inflammatory arthritis...
  9. ncbi request reprint Role of cell-matrix interactions in osteoclast differentiation
    K P McHugh
    Department of Orthopaedics and Rheumatology, Beth Israel Deaconess Medical Center, New England Baptist Hospital, and New England Baptist Bone and Joint Institute, Harvard Medical School, Boston, MA, USA
    Adv Exp Med Biol 602:107-11. 2007
    ..They also share a common lineage..
  10. pmc The role of TNF-receptor family members and other TRAF-dependent receptors in bone resorption
    E M Gravallese
    Beth Israel Deaconess Medical Center, New England Baptist Bone and Joint Institute, Harvard Institutes of Medicine, Harvard Medical School, Boston, MA 02115, USA
    Arthritis Res 3:6-12. 2001
    ....
  11. pmc NFATc1 directly induces the human beta3 integrin gene in osteoclast differentiation
    T N Crotti
    Beth Israel Deaconess Medical Center, Boston, MA 02115, USA
    J Musculoskelet Neuronal Interact 5:335-7. 2005
  12. pmc TRANCE/RANKL knockout mice are protected from bone erosion in a serum transfer model of arthritis
    A R Pettit
    Beth Israel Deaconess Medical Center, New England Baptist Bone and Joint Institute, Harvard Institutes of Medicine, Boston, Massachusetts 02115, USA
    Am J Pathol 159:1689-99. 2001
    ..These results confirm the central role of osteoclasts in the pathogenesis of bone erosion in arthritis and demonstrate distinct mechanisms of cartilage destruction and bone erosion in this animal model of arthritis...
  13. pmc NFATc1 regulation of the human beta3 integrin promoter in osteoclast differentiation
    Tania N Crotti
    Beth Israel Deaconess Medical Center, Boston, MA 02115, USA
    Gene 372:92-102. 2006
    ..Together these results establish the beta3 gene as a direct target of NFATc1 in RANKL-dependent osteoclast formation...
  14. ncbi request reprint Rheumatic diseases: the effects of inflammation on bone
    Nicole C Walsh
    Beth Israel Deaconess Medical Center, New England Baptist Bone and Joint Institute, Harvard Institutes of Medicine, Boston, MA 02115, USA
    Immunol Rev 208:228-51. 2005
    ..In this review, we provide an overview of the cell types, inflammatory mediators, and mechanisms that are implicated in bone loss and new bone formation in inflammatory joint diseases...
  15. ncbi request reprint A novel promoter regulates calcitonin receptor gene expression in human osteoclasts
    Zhenxin Shen
    New England Baptist Bone and Joint Institute, Boston, MA 02120, USA
    Biochim Biophys Acta 1769:659-67. 2007
    ....
  16. ncbi request reprint Bisphosphonates: environmental protection for the joint?
    Steven R Goldring
    Arthritis Rheum 50:2044-7. 2004
  17. pmc Amylin inhibits bone resorption while the calcitonin receptor controls bone formation in vivo
    Romain Dacquin
    Department of Molecular and Human Genetics and Bone Disease Program of Texas, Baylor College of Medicine, One Baylor Plaza, Room S921, Houston, TX 77030, USA
    J Cell Biol 164:509-14. 2004
    ..Thus, amylin is a physiological regulator of bone resorption that acts through an unidentified receptor...
  18. ncbi request reprint ESE-1 is a novel transcriptional mediator of angiopoietin-1 expression in the setting of inflammation
    Courtney Brown
    Beth Israel Deaconess Medical Center, Department of Medicine, New England Baptist Bone and Joint Institute, Harvard Institutes of Medicine, 4 Blackfan Circle, Boston, MA 02115, USA
    J Biol Chem 279:12794-803. 2004
    ..Our results support a novel paradigm for the ETS factor ESE-1 as a transcriptional mediator of angiogenesis in the setting of inflammation...
  19. doi request reprint PU.1 and NFATc1 mediate osteoclastic induction of the mouse beta3 integrin promoter
    Tania N Crotti
    The New England Baptist Bone and Joint Institute, Department of Rheumatology, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, Massachusetts 02115, USA
    J Cell Physiol 215:636-44. 2008
    ..1, are involved in regulation of beta(3) integrin expression during osteoclast differentiation and suggest that PU.1 confers specificity to the NFATc1 response to macrophage lineage cells...
  20. ncbi request reprint Responses to the proinflammatory cytokines interleukin-1 and tumor necrosis factor alpha in cells derived from rheumatoid synovium and other joint tissues involve nuclear factor kappaB-mediated induction of the Ets transcription factor ESE-1
    Franck Grall
    New England Baptist Bone and Joint Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, and Beth Israel Deaconess Medical Center Genomics Center, Boston, Massachusetts 02115, USA
    Arthritis Rheum 48:1249-60. 2003
    ....
  21. doi request reprint The role of bone in osteoarthritis pathogenesis
    Steven R Goldring
    The Hospital for Special Surgery, Weill Medical College of Cornell University, 535 East 70th Street, New York, NY 10021, USA
    Rheum Dis Clin North Am 34:561-71. 2008
    ..In addition, the relationship of these changes to the alterations in articular cartilage and the other tissues comprising the diarthrodial joint are reviewed...
  22. ncbi request reprint Increase in expression of receptor activator of nuclear factor kappaB at sites of bone erosion correlates with progression of inflammation in evolving collagen-induced arthritis
    Erik Lubberts
    University Medical Center Nijmegen, Nijmegen, The Netherlands
    Arthritis Rheum 46:3055-64. 2002
    ..This study was undertaken to identify in vivo the hitherto-unknown origin and localization of RANK-expressing osteoclast precursor cells at sites of bone erosion in arthritis...
  23. ncbi request reprint Comparison of cathepsins K and S expression within the rheumatoid and osteoarthritic synovium
    Wu Shiun Hou
    Mount Sinai School of Medicine, New York, New York 10029, USA
    Arthritis Rheum 46:663-74. 2002
    ....
  24. pmc The role played by cell-substrate interactions in the pathogenesis of osteoclast-mediated peri-implant osteolysis
    Zhenxin Shen
    New England Baptist Bone and Joint Institute, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
    Arthritis Res Ther 8:R70. 2006
    ..We speculate that, in addition to the role of cytokines and growth factors, the substrate with which these cells interact plays a critical role in their differential phenotypic and functional properties...
  25. ncbi request reprint Osteoarthritis
    Mary B Goldring
    Laboratory for Cartilage Biology, Research Division, The Hospital for Special Surgery, Weill College of Medicine of Cornell University, New York 10021, USA
    J Cell Physiol 213:626-34. 2007
    ....
  26. ncbi request reprint The role of adsorbed endotoxin in particle-induced stimulation of cytokine release
    David R Cho
    Harvard Institutes of Medicine, Rheumatology Division, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA
    J Orthop Res 20:704-13. 2002
    ..Furthermore, the presence of particle-associated endotoxin at the bone-implant interface in vivo could markedly enhance the adverse biological activity of particulate wear debris...
  27. ncbi request reprint Relationship between cartilage stiffness and dGEMRIC index: correlation and prediction
    Marta Baldassarri
    New England Baptist Bone and Joint Institute, Boston, Massachusetts, USA
    J Orthop Res 25:904-12. 2007
    ..A generalized relationship was found to provide good correspondence across sources and regions. Use of the dGEMRIC index as a predictive measure of stiffness is possible, depending on the application's acceptable error...
  28. ncbi request reprint Eating bone or adding it: the Wnt pathway decides
    Steven R Goldring
    Nat Med 13:133-4. 2007
  29. pmc Novel dexamethasone-HPMA copolymer conjugate and its potential application in treatment of rheumatoid arthritis
    Dong Wang
    Department of Pharmaceutical Sciences, College of Pharmacy, University of Nebraska Medical Center, Omaha, NE 68198 6025, USA
    Arthritis Res Ther 9:R2. 2007
    ..This newly developed drug delivery system provides a unique method for selective targeting of glucocorticoids to inflamed joints which may potentially reduce systemic side effects...
  30. ncbi request reprint The Ets transcription factor ESE-1 mediates induction of the COX-2 gene by LPS in monocytes
    Franck T Grall
    New England Baptist Bone and Joint Institute and BIDMC Genomics Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115, USA
    FEBS J 272:1676-87. 2005
    ....
  31. ncbi request reprint Gene expression clustering using self-organizing maps: analysis of the macrophage response to particulate biomaterials
    Grant E Garrigues
    Biomaterials Laboratory, Massachusetts General Hospital, Harvard Medical School, GRJ 1115, 55 Fruit Street, Boston, MA 02114, USA
    Biomaterials 26:2933-45. 2005
    ..We also uncovered a novel set of genes, which not only validates and logically extends the current model of the pathogenesis of osteolysis and aseptic loosening, but also provides new targets for further research and therapeutics...
  32. ncbi request reprint Microscopic metallic wear and tissue response in failed titanium hallux metatarsophalangeal implants: two cases
    Navid Ghalambor
    The Hand Care Center, Orange, California, USA
    Foot Ankle Int 23:158-62. 2002
    ....
  33. ncbi request reprint Nitric oxide promotes infectious bone resorption by enhancing cytokine-stimulated interstitial collagenase synthesis in osteoblasts
    Sze Kwan Lin
    Department of Dentistry, National Taiwan University Hospital, Taipei, Taiwan
    J Bone Miner Res 18:39-46. 2003
    ..These data suggest that NO derived from macrophages after LPS stimulation may enhance bone loss by augmenting the cytokine-induced MMP-1 production in osteoblasts...
  34. ncbi request reprint MEK/ERK and signal transducer and activator of transcription signaling pathways modulate oncostatin M-stimulated CCL2 expression in human osteoblasts through a common transcription factor
    Sze Kwan Lin
    National Taiwan University Hospital, Taipei, Taiwan
    Arthritis Rheum 50:785-93. 2004
    ..To analyze the effects of oncostatin M (OSM), a gp130-type cytokine, on CCL2 expression in MG-63 cells, a human osteosarcoma cell line with a characteristic osteoblastic phenotype, and to investigate the signaling pathway involved...