Abstracts tagged "rheumatoid arthritis (RA) and synovial cells"

Abstract Number: 1576 • 2016 ACR/ARHP Annual Meeting
Identifying Rheumatoid Arthritis Subtypes Using Synovial Tissue Gene Expression Profiling, Histologic Scoring and Clinical Correlates
Dana E. Orange¹, Susan M. Goodman², Phaedra Agius³, Ryan Cummings⁴, Kathleen Andersen¹, Robert Darnell⁵, Lionel Ivashkiv², Alessandra B. Pernis⁶, Edward F. DiCarlo⁷, Vivian P. Bykerk⁸ and Laura T. Donlin⁹, ¹Rheumatology, Hospital for Special Surgery, New York, NY, ²Medicine, Hospital for Special Surgery, New York, NY, ³New York Genome Center, New York, NY, ⁴Hospital for Special Surgery, New York, NY, ⁵The New York Genome Center, New York, NY, ⁶David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY, ⁷Laboratory Medicine, Hospital for Special Surgery, New York, NY, ⁸Divison of Rheumatology, Hospital for Special Surgery, New York, NY, ⁹Arthritis and Tissue Degeneration Program and the David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY
Background/Purpose: The histopathologic features of synovial tissue vary widely among patients with rheumatoid arthritis (RA) undergoing arthroplasty and the clinical significance of this variability is…
Abstract Number: 2156 • 2016 ACR/ARHP Annual Meeting
IL-6 and TNF-α Modulate Expressions of Cell Cycle Regulators of Rheumatoid Arthritis Fibroblast-like Synoviocytes
Kenta Kaneshiro¹, Teppei Hashimoto², Kohsuke Yoshida¹, Ayako Nakai¹, Naonori Hashimoto¹, Kohjin Suzuki¹, Koto Uchida¹, Yoshiko Kawasaki², Natsuko Nakagawa³, Nao Shibanuma⁴, Yoshitada Sakai⁵ and Akira Hashiramoto⁶, ¹Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan, ²Department of Rheumatology, Kobe Kaisei Hospital, Kobe, Japan, ³Department of Orthopaedic Surgery, Konan-Kakogawa Hospital, Kakogawa, Japan, ⁴Departmant of Orthopaedic Surgery, Kobe Kaisei Hospital, Kobe, Japan, ⁵Division of Rehabilitation Medicine, Kobe University Graduate School of Medicine, Kobe, Japan, ⁶Department of Biophysics, Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan
Background/Purpose: Iinterleukin(IL)-6 and tumor necrosis factor(TNF)-α play important roles in the pathogenesis of RA, however, it remains unclear how they affect or modulate the…
Abstract Number: 2561 • 2016 ACR/ARHP Annual Meeting
A Novel Pharmacological Action of MTX on RA Fibroblast-like Synoviocytes Via Circadian Clock Genes
Kohjin Suzuki¹, Kohsuke Yoshida¹, Teppei Hashimoto², Kenta Kaneshiro¹, Ayako Nakai¹, Naonori Hashimoto¹, Yoshiko Kawasaki², Nao Shibanuma³, Natsuko Nakagawa⁴, Yoshitada Sakai⁵ and Akira Hashiramoto⁶, ¹Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan, ²Department of Rheumatology, Kobe Kaisei Hospital, Kobe, Japan, ³Departmant of Orthopaedic Surgery, Kobe Kaisei Hospital, Kobe, Japan, ⁴Department of Orthopaedic Surgery, Konan-Kakogawa Hospital, Kakogawa, Japan, ⁵Division of Rehabilitation Medicine, Kobe University Graduate School of Medicine, Kobe, Japan, ⁶Department of Biophysics, Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan
Background/Purpose: The circadian rhythm is disrupted in patients with rheumatoid arthritis (RA), and we have shown that tumor necrosis factor(TNF)-ƒ¿ inhibits the expression of circadian…
Abstract Number: 3216 • 2016 ACR/ARHP Annual Meeting
Integrated High-Dimensional Analyses Reveal a Pathologically Expanded ‘Peripheral’ B Cell-Helper T Cell Population in Rheumatoid Arthritis
Deepak Rao¹, Michael Gurish², Kamil Slowikowski³, Chamith Fonseka², Jennifer Marshall⁴, Yanyan Liu⁵, Laura T. Donlin⁶, Lauren Henderson⁷, Fumitaka Mizoguchi⁸, Nikola Teslovich⁹, Michael Weinblatt¹⁰, Elena Massarotti¹⁰, Jonathan Coblyn¹¹, Simon M. Helfgott¹⁰, Yvonne C. Lee¹², Derrick J. Todd¹⁰, Vivian P. Bykerk¹³, Susan M. Goodman¹⁴, Alessandra B. Pernis¹⁵, Lionel Ivashkiv¹⁴, Elizabeth W. Karlson¹⁰, Peter Nigrovic⁹, Andrew Filer¹⁶, Christopher Buckley¹⁷, James Lederer¹⁸, Soumya Raychaudhuri¹⁹ and Michael Brenner¹, ¹Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, ²Division of Rheumatology, Immunology, Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, ³Divisions of Rheumatology and Genetics, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, ⁴Rheumatology Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, United Kingdom, ⁵Brigham and Women's Hospital and Harvard Medical School, Boston, MA, ⁶Arthritis and Tissue Degeneration Program and the David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY, ⁷Division of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, ⁸Department of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan, ⁹Brigham and Women's Hospital and Harvard Medical School, Cambridge, MA, ¹⁰Rheumatology, Immunology and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, ¹¹Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, ¹²Rheumatology Immunology & Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, ¹³Divison of Rheumatology, Hospital for Special Surgery, New York, NY, ¹⁴Medicine, Hospital for Special Surgery, New York, NY, ¹⁵David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY, ¹⁶University of Birmingham, Birmingham, United Kingdom, ¹⁷Rheumatology, University of Birmingham, Birmingham, United Kingdom, ¹⁸Department of Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, ¹⁹Brigham and Women's Hospital, Boston, MA
Background/Purpose: Determining the pathologic functions of T cells that infiltrate target tissues remains a central challenge in autoimmune diseases. In rheumatoid arthritis (RA), the formation…
Abstract Number: 3218 • 2016 ACR/ARHP Annual Meeting
Synovial Mast Cells Associate with High Disease Activity and Predict Radiographic Progression at 12 Months in Patients with Early Rheumatoid Arthritis
Felice Rivellese¹, Frances Humby¹, Stephen Kelly¹, Amato de Paulis², Gianni Marone² and Costantino Pitzalis¹, ¹Centre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and The London, School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom, ²Department of Translational Medical Sciences and Center for Basic and Clinical Immunology Research (CISI), University of Naples Federico II, Naples, Italy
Background/Purpose: Mast cells (MCs) are immune cells present in the synovial membrane and implicated in the pathogenesis of Rheumatoid Arthritis, although their exact contribution…
Abstract Number: 2569 • 2015 ACR/ARHP Annual Meeting
Regulation of SIRT1 Maybe a Perfect Strategy in Treatment of Rheumatoid Arthritis
Sang-Yeob Lee¹, Sung Won Lee², Won Tae Chung², Jae Ho Bae³, So Youn Park⁴ and Chi Dae Kim⁴, ¹Division of Rheumatology, Department of Internal Medicine, Dong-A University College of Medicine, Busan, South Korea, ²Rheumatology, Dong-A University Hospital, Busan, South Korea, ³Biochemistry, Pusan national university, Yong -San, South Korea, ⁴Medical Research Center for Ischemic Tissue Regeneration, Pusan national university, Yong -San, South Korea
Background/Purpose: Monocyte may differentiate to osteoclasts in bone and macrophages in joint. so, blocking of monocyte differentiation maybe effective target in RA (rheumatoid arthritis) treatment.…
Abstract Number: 2703 • 2015 ACR/ARHP Annual Meeting
Reduction in Matrix Metalloproteinase-1 and -2 Secretion from Fibroblast-like Synoviocytes after Induction of Adipogenesis By a Natural Peroxisome Proliferator-Activated Receptor Gamma Ligand, Arterpilin-C
Eiji Sugiyama¹, Satoshi Yamasaki¹ and Je-Tae Woo^2,3, ¹Department of Clinical Immunology and Rheumatology, Hiroshima University Hospital, Hiroshima, Japan, ²Department of Biological Chemistry, Chubu University, Aichi, Japan, ³JT WOO, Okinawa Research Center Co., Ltd, Okiawa, Japan
Background/Purpose: Fibroblast-like synoviocytes (FLS) play important roles in rheumatoid arthritis (RA) by producing matrix metalloproteinase (MMP) and cytokines, and hence, these cells are a therapeutic…
Abstract Number: 3104 • 2015 ACR/ARHP Annual Meeting
Abnormal DNA Methylation in a Novel PTPN11 Enhancer Increases Destructive Potential of Rheumatoid Arthritis (RA) Fibroblast-like Synoviocytes (FLS) and Joint Inflammation
Keisuke Maeshima¹, Stephanie M. Stanford², Deepa Hammaker¹, Cristiano Sacchetti², Rizi Ai³, Vida Zhang⁴, David L. Boyle⁵, Lifan Zeng⁶, German Muench⁷, Gen-Sheng Feng⁸, John Whitaker⁹, Zhong-Yin Zhang⁶, Wei Wang¹⁰, Nunzio Bottini² and Gary S. Firestein⁵, ¹Division of Rheumatology, Allergy and Immunology, UCSD School of Medicine, La Jolla, CA, ²Cellular Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA, ³Chemistry and Biochemistry, UC San Diego, La Jolla, CA, ⁴Division of Cellular Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA, ⁵Division of Rheumatology, Allergy and Immunology, University of California, San Diego, La Jolla, CA, ⁶Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, ⁷La Jolla Institute for Allergy and Immunology, La Jolla, CA, ⁸Pathology and Division of Biological Sciences, UC San Diego, La Jolla, CA, ⁹Janssen Pharmaceuticals, La Jolla, CA, ¹⁰Chemistry and Biochemistry, University of California, San Diego, La Jolla, CA
Background/Purpose: Rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS) mediate disease pathogenesis by invading the joint extracellular matrix. The PTPN11 gene, encoding the tyrosine phosphatase SHP-2, is overexpressed…
Abstract Number: 4 • 2015 ACR/ARHP Annual Meeting
The Influence of Adipokines on the Interaction of Rheumatoid Arthritis Synovial Fibroblasts with Endothelial Cells
Rebecca Hasseli¹, Klaus W. Frommer², Thomas Dr. Umscheid³, Markus Prof. Dr. Schönburg⁴, Stefan Rehart⁵, Ulf Müller-Ladner² and Elena Neumann², ¹Justus-Liebig-University of Giessen, Kerckhoff-Klinik, Bad Nauheim, Germany, ²Internal Medicine and Rheumatology, Justus-Liebig-University of Giessen, Kerckhoff-Klinik, Bad Nauheim, Germany, ³William Harvey Klinik; Bad Nauheim, Germany, Bad Nauheim, Germany, ⁴Department of Cardiac Surgery; Kerckhoff-Klinik, Bad Nauheim, Bad Nauheim, Germany, ⁵Orthopedics and Trauma Surgery, Markus-Hospital, Frankfurt, Germany
Background/Purpose: Rheumatoid Arthritis (RA) is a systemic chronic inflammatory disease. Adipose tissue, being an endocrine organ, plays an important role in inflammatory processes. Adipokines are…
Abstract Number: 12 • 2015 ACR/ARHP Annual Meeting
Delta-like 1 Enhances the Production of Pro-Inflammatory Mediators By Fibroblast-like Synoviocytes
Chiyoko Sekine, Department of Clinical Research Medicine, Teikyo University School of Medicine, Tokyo, Japan
Background/Purpose: Notch signaling is known to regulate cell fate decision and differentiation during embryonic and post-natal development. I have been reported that a Notch ligand…
Abstract Number: 1035 • 2015 ACR/ARHP Annual Meeting
Synovium-Derived microRNAs Inhibit Bone Formation in Rheumatoid Arthritis
Ellen M. Gravallese¹, Yukiko Maeda², Nicholas H Farina³, Paul Fanning⁴ and Jane Lian³, ¹Lazare Research Bldg Ste 223, University of Massachusetts Medical School, Worcester, MA, ²Medicine, University of Massachusetts Medical School, Worcester, MA, ³Department of Biochemistry, University of Vermont, Burlington, VT, ⁴Department of Orthopedics, University of Massachusetts Medical School, Worcester, MA
Background/Purpose: Articular bone erosion in rheumatoid arthritis (RA) is a consequence of synovial inflammation that leads to disability for patients. Cells within the synovium secrete…
Abstract Number: 1098 • 2015 ACR/ARHP Annual Meeting
Interleukin-1 Reciprocally Regulates Interferon-Gamma Induced B Cell Activating Factor of the Tumor Necrosis Factor Family (BAFF) and Interleukin-6 in Human Synovial Fibroblasts
Georg Pongratz¹, Rainer Straub² and Torsten Lowin³, ¹Rheumatology - Hiller Research Center Rheumatology, University Hospital Düsseldorf, Düsseldorf, Germany, ²Laboratory of Experimental Rheumatology and Neuroendocrine Immunology, Department of Internal Medicine, University Hospital Regensburg, Regensburg, Germany, ³Internal Medicine I, University Hospital Regensburg, Regensburg, Germany
Background/Purpose: B cell activating factor of the tumor necrosis factor family (BAFF) and interleukin-6 (IL-6) are cytokines important for the stimulation and survival of autoreactive…
Abstract Number: 1627 • 2015 ACR/ARHP Annual Meeting
HIF-1alpha Knockdown Down-Regulates Glycolytic Metabolism and Induces Rheumatoid Synovial Fibroblast Cell Death
Manuel J. Del Rey¹, Alicia Usategui¹, Álvaro Valín¹, María Sánchez-Aragó², José M. Cuezva², Carmen M. García-Herrero¹, María Galindo¹, Juan D. Cañete³, Francisco J. Blanco⁴, Gabriel Criado¹ and Jose L. Pablos¹, ¹Servicio de Reumatología, Instituto de Investigación Hospital 12 de Octubre (i+12), Madrid, Spain, ²Departamento de Biología Molecular, Centro de Biología Molecular Severo Ochoa, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Instituto de Investigación Hospital 12 de Octubre, Universidad Autónoma de Madrid, Madrid, Spain, ³Unitat d’Artritis, Servei de Reumatologia, Hospital Clínic de Barcelona and Institut d’Investigacions Biomèdiques August Pí i Sunyer, Barcelona, Spain, ⁴Laboratorio de Investigación Osteoarticular y del Envejecimiento, Instituto de Investigación Biomédica de A Coruña, INIBIC, A Coruña, Spain
Background/Purpose: Intense synovial fibroblast (SF) hyperplasia contributes to the chronic inflammation and osteoarticular destruction that characterizes rheumatoid arthritis (RA). Hypoxia-inducible factor 1α (HIF-1α) plays a…
Abstract Number: 2133 • 2015 ACR/ARHP Annual Meeting
Receptor Protein Tyrosine Phosphatase Alpha Enhances Rheumatoid Synovial Fibroblast Signaling and Promotes Arthritis in Mice
Stephanie M. Stanford¹, Mattias N. D. Svensson¹, Cristiano Sacchetti¹, Caila A. Pilo¹, Dennis J. Wu¹, William B. Kiosses², Annelie Hellvard³, Brith Bergum³, German R. Aleman Muench¹, Christian Elly¹, Yun-Cai Liu¹, Jeroen den Hertog^4,5, Ari Elson⁶, Jan Sap⁷, Piotr Mydel³, David L. Boyle⁸, Maripat Corr⁸, Gary S. Firestein⁸ and Nunzio Bottini¹, ¹Cellular Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA, ²The Scripps Research Institute, La Jolla, CA, ³Clinical Science, Broegelmann Research Laboratory, Bergen, Norway, ⁴Hubrecht Institute-Koninklijke Nederlands Akademie van Wetenschappen and University Medical Center Utrecht, Utrecht, Netherlands, ⁵Institute of Biology Leiden, Leiden, Netherlands, ⁶Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel, ⁷Epigenetics and Cell Fate, Université Paris Diderot Sorbonne Paris Cité, Paris, France, ⁸Division of Rheumatology, Allergy and Immunology, University of California at San Diego School of Medicine, La Jolla, CA
Background/Purpose: Rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS) promote disease pathogenesis by aggressively invading the joint extracellular matrix. The focal adhesion kinase (FAK) signaling pathway is…
Abstract Number: 2818 • 2014 ACR/ARHP Annual Meeting
SH2 Domain-Containing Phosphatase 2 Promotes Aggressiveness of Rheumatoid Fibroblast-like Synoviocytes
Stephanie M. Stanford¹, German R. Aleman Muench¹, Cristiano Sacchetti¹, Lifan Zeng², David L. Boyle³, Gen-Sheng Feng⁴, Zhong-Yin Zhang², Maripat Corr³, Gary S. Firestein³ and Nunzio Bottini¹, ¹Cellular Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA, ²Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, ³Division of Rheumatology, Allergy and Immunology, University of California at San Diego School of Medicine, La Jolla, CA, ⁴Pathology, University of California at San Diego Division of Biological Sciences, La Jolla, CA
Background/Purpose In rheumatoid arthritis (RA), fibroblast-like synoviocytes (FLS) that line joint synovial membranes aggressively invade the extracellular matrix, destroying cartilage and bone. Although this cell…

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