ACR Meeting Abstracts

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Abstracts tagged "Apoptosis"

  • Abstract Number: 1728 • 2013 ACR/ARHP Annual Meeting

    Amelioration Of Collagen-Induced Arthritis By Modulation Of Inhibitory Apoptosis Stimulating Protein Of p53 To Activate Transcription Factor p73

    Chrong-Reen Wang1, Shih-Yao Chen2, Ai-Li Shiau3, Yuan-Tsung Li4, Chia-Tse Weng5, I-Ming Jou6, Ming-Fei Liu7 and Chao-Liang Wu2, 1Section of Rheumatology and Immunology, Department of Internal Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan, 2Biochemistry and Molecular Biology, National Cheng Kung University Medical College, Tainan, Taiwan, 3Microbiology and Immunology, National Cheng Kung University Medical College, Tainan, Taiwan, 4Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, 5Internal Medicine, National Cheng Kung University Medical College, Tainan, Taiwan, 6Orthopedics, National Cheng Kung University Medical College, Tainan, Taiwan, 7Internal Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan

    Background/Purpose: Our previous studies have demonstrated p53 mutations competent for the inactivation of wild type p53 in synovial fibroblasts (SF) from either rheumatoid arthritis patients…
  • Abstract Number: 1406 • 2013 ACR/ARHP Annual Meeting

    The Scaffold Protein p62 Is Involved In NF-κB Signaling, Caspase-3 Dependent and -Independent Cell Death and Autophagy In Rheumatoid Arthritis Synovial Fibroblasts

    Masaru Kato1, Caroline Ospelt1, Christoph Kolling2, Beat A. Michel3, Renate E. Gay4, Steffen Gay5 and Kerstin Klein1, 1Center of Experimental Rheumatology, University Hospital Zurich, Zurich, Switzerland, 2Schulthess Clinic, Zurich, Switzerland, 3Department of Rheumatology, University Hospital Zurich, Zurich, Switzerland, 4Center of Experimental Rheumatology, Zurich University Hospital, Zurich, Switzerland, 5Center of Experimental Rheumatology, University Hospital Zurich and Zurich Center of Integrative Human Physiology (ZIHP), Zurich, Switzerland

    Background/Purpose: Sequestosome 1 (p62/ SQSTM1) is a multifunctional ubiquitin-binding protein implicated in selective autophagy, cell signaling pathways and regulation of cell death. Recently, we described…
  • Abstract Number: 1392 • 2013 ACR/ARHP Annual Meeting

    The Expression Of Proto-Oncogene Survivin Splicing Variant 2B In Synovial Tissues and Blood From Patients With Rheumatoid Arthritis

    Sho Mokuda1,2, Tatsuhiko Miyazaki3, Junya Masumoto3, Masamoto Kanno4 and Kiyoshi Takasugi5, 1Department of Immunology, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan, 2Department of Internal Medicine, Center for Rheumatic Diseases, Dohgo Spa Hospital, Matsuyama, Japan, 3Department of Pathology, Division of Analyticalpathology, Ehime University Graduate School of Medicine, Toon, Japan, 4Department of Immunology, Graduate School of Biomedical Sciences, Hiroshima University, Hirosima, Japan, 5Center for Rheumatic Diseases, Dohgo Spa Hospital, Matsuyama, Japan

    Background/Purpose: It has been reported that serum survivin level was an independent risk factor for predicting joint destruction in early rheumatoid arthritis (RA). The proto-oncogene…
  • Abstract Number: 939 • 2013 ACR/ARHP Annual Meeting

    Reduction Of Circulating Blood Neutrophils In Mice By Anti-IL-6R Alpha Monoclonal Antibody is Not Due To Apoptosis Or Blockade Of Neutrophil Differentiation

    Ludmila Kelly, Vilma Decman and Dimitris Skokos, Research, Regeneron Pharmaceuticals, Inc., Tarrytown, NY

    Background/Purpose: Blockade of IL-6/IL-6Rα signaling is associated with a reduction of circulating neutrophils in the blood of patients treated with anti-IL-6Rα mAb but the mechanism…
  • Abstract Number: 569 • 2013 ACR/ARHP Annual Meeting

    Hydroxycholorquine Is Cardioprotective In Neonatal Rat Cardiomyocytes Exposed To Simulated Myocardial Ischaemic/Reperfusion Injury.-An Effect Mediated Through ERK Phosphorylation

    Lauren Bourke1, James McCormick2, Anastasis Stephanou3 and Yiannis Ioannou4, 1Centre for Rheumatology Research, University College London, London, United Kingdom, 2Clinical & Molecular Genetics Unit, University College London, London, United Kingdom, 3MMBU, University College London, London, United Kingdom, 4Arthritis Research UK Centre for Adolescent Rheumatology at University College London, Great Ormond Street Hospital and UCLH, University College London, London, United Kingdom

    Background/Purpose: A significant amount of myocardial damage during a myocardial infarction (MI) occurs during the reperfusion stage which is known as ischaemic reperfusion (I/R) injury…
  • Abstract Number: 546 • 2013 ACR/ARHP Annual Meeting

    The Survival Of Gr1+CD11b+ cells Is Differentially Regulated In Male and Female Lupus-Prone Mice

    Elena Gonzalez1,2, Trine Jorgensen2 and Abhishek Trigunaite2, 1Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, 2Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH

    Background/Purpose: Systemic Lupus Erythematosis (SLE) is a multisystem autoimmune disease that develops far more frequently in females than in males (9:1 ratio). The (NZBxNZW)F1 lupus-prone…
  • Abstract Number: 551 • 2013 ACR/ARHP Annual Meeting

    Different Cell Death Programs Contribute To Severity Of Lupus Glomerulonephritis In Males and Females

    Neelakshi Jog1 and Roberto Caricchio2, 1Rheumatology, Temple University, Philadelphia, PA, 2Medicine/Rheumatology, Temple University, Philadelphia, PA

    Background/Purpose: Lupus glomerulonephritis (GN) is a leading cause of long-term disability in SLE. Although lupus is more common in females, GN occurs earlier and in…
  • Abstract Number: 555 • 2013 ACR/ARHP Annual Meeting

    Therapeutic Inhibition Of Anti-Apoptotic BCL-2 Family Proteins In a Murine Model Of Lupus Nephritis

    Li Chun Wang1, Stuart Perper2, Danise Perron3, Edit Tarcsa4, Philip Bardwell3, Neelufar Mozaffarian5, Andrew Souers5, Steven Elmore6, Tariq Ghayur7 and Lisa Olson3, 1Immunology, AbbVie Inc, AbbVie Bioresearch Center, Worcester, MA, 2Pharmacology, AbbVie Bioresearch Center, Inc, Worcester, MA, 3Immunology, AbbVie Bioresearch Center, Inc, Worcester, MA, 4Immunology, AbbVie Bioresearch Center, Worcester, MA, 5AbbVie, North Chicago, IL, 6AbbVie Inc, North Chicago, IL, 7AbbVie Bioresearch Center, Inc, Worcester, MA

    Background/Purpose: Apoptosis is both a conserved and highly regulated process that is essential for normal development and tissue homeostasis. This process, also known as programmed…
  • Abstract Number: 560 • 2013 ACR/ARHP Annual Meeting

    Purified IgG From Patients With Systemic Lupus Erythematosus Enhances Apoptosis In Neonatal Rat Cardiomyocytes Exposed To Simulated Myocardial Ischaemic/Reperfusion Injury

    Lauren Bourke1, James McCormick2, Vera Ripoll3, Charis Pericleous4, Anna Radziszewska5, Anastasis Stephanou6 and Yiannis Ioannou7, 1Centre for Rheumatology Research, University College London, London, United Kingdom, 2Clinical & Molecular Genetics Unit, University College London, London, United Kingdom, 3Centre for Rheumatology Research, Division of Medicine, University College London, London, United Kingdom, 4Centre for Rheumatology, Division of Medicine, Centre for Rheumatology, University College London, London, United Kingdom, 5The Rayne Institute, Arthritis Research UK Centre for Adolescent Rheumatology at University College London, Great Ormond Street Hospital and UCLH, University College London, London, United Kingdom, 6Medical and Molecular Biology Unit (MMBU), University College London, London, United Kingdom, 7Arthritis Research UK Centre for Adolescent Rheumatology at University College London, Great Ormond Street Hospital and UCLH, University College London, London, United Kingdom

    Background/Purpose: A significant amount of myocardial damage during a myocardial infarction (MI) occurs during the reperfusion stage which is known as ischaemic reperfusion (I/R) injury…
  • Abstract Number: 2679 • 2012 ACR/ARHP Annual Meeting

    Loss of Caspase 8 in Dendritic Cells Induces a Systemic Lupus Erythematosus-Like Disease That Is Independent of the Necroptosome

    Carla M. Cuda1, Alexander V. Misharin2, Rana Saber2, G. Kenneth Haines III3, Jack Hutcheson4, Chandra Mohan5 and Harris R. Perlman6, 1Medicine / Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL, 2Medicine/Rheumatology, Northwestern University, Chicago, IL, 3Department of Pathology, Yale University, New Haven, CT, 4Internal Medicine - Rheumatic Diseases, University of Texas Southwestern Medical Center, Dallas, TX, 5Internal Medicine/Division of Rheumatology, University of Texas Southwestern Medical Center, Dallas, TX, 6Feinberg School of Medicine, Northwestern University, Chicago, IL

    Background/Purpose: Systemic lupus erythematosus (SLE) is a multi-organ, destructive autoimmune disease characterized by pathogenic autoantibodies.  Though it is accepted that dendritic cells (DCs) play an…
  • Abstract Number: 2325 • 2012 ACR/ARHP Annual Meeting

    PD-1 Signaling Promotes Suppressive Function of CD4+ Regulatory T Cells in (New Zealand Black x New Zealand White )F1 Lupus-Prone Mice in a Dose-Dependent Manner

    Maida Wong1, Antonio La Cava2 and Bevra H. Hahn3, 1Internal Medicine/Rheumatology, University of California, Los Angeles, Los Angeles, CA, 2Internal Medicine/Rheumatology, UCLA David Geffen School of Medicine, Los Angeles, CA, 3Rheumatology, UCLA David Geffen School of Medicine, Los Angeles, CA

    Background/Purpose: Programmed death-1 (PD-1) has been regarded as a negative regulatory signal in T cells. Our laboratory has shown that PD-1 is important in T…
  • Abstract Number: 2296 • 2012 ACR/ARHP Annual Meeting

    Platelet Release Products Mediate Endothelial Apoptosis: A Possible Role for Thrombospondin 1- CD36 Pathway in SSc-Endothelial Apoptosis

    Bashar Kahaleh1 and Yongqing Wang2, 1Medicine/Rheumatology, University of Toledo, Toledo, OH, 2Medicine, University of Toledo, Toledo, OH

    Background/Purpose: Sequential pathologic observations in the early stages of SSc demonstrated evidence for platelet aggregation and binding to blood vessels that is generally followed by…
  • Abstract Number: 2083 • 2012 ACR/ARHP Annual Meeting

    New Treatment Approach of Rheumatoid Arthritis Based On Inhibition of Cyclin Dependent Kinase-9

    Annelie Hellvard1, Lutz Zeitlmann2, Ulrich Heiser3, André Niestroj3, Hans-Ulrich Demuth3, Jan Potempa4 and Piotr Mydel1, 1Broegelmann Research Laboratory, The Gade Institute, University of Bergen, Bergen, Norway, 2Ingenium Pharmaceuticals GmbH, Martinsried, Germany, 3Probiodrug AG, Halle/Saale, Germany, 4Microbiology Department, Jagiellonian University, Krakow, Poland

    Background/Purpose: Cyclin dependent kinase-9 (cdk-9) is transcription regulator of the carboxyterminal domain of RNA polymerase II. The usage of pan-cdk inhibitors such as flavopiridol has…
  • Abstract Number: 1782 • 2012 ACR/ARHP Annual Meeting

    Dual Effects of Soluble FasL and Membrane Bound FasL On Fibroblast-Like Synoviocytes Cells (FLS) From Rheumatoid Arthritis (RA) Patients

    Rachel Audo1, Flavia Calmon-Hamaty1, Bernard Combe2, Michael Hahne1 and Jacques Morel3, 1IGMM, CNRS UMR5535, Montpellier, Montpellier, France, 2Rheumatology, Hopital Lapeyronie, Montpellier, France, 3Dpartment of Rheumatology, Lapeyronie Hospital, Montpellier, France

    Background/Purpose: Membrane bound FasL (mFasL) is able to induce fibroblast-like synoviocytes (FLS) cell death. In experimental arthritis mouse models, injection of agonistic antibody  (Ab) anti-Fas…
  • Abstract Number: 1776 • 2012 ACR/ARHP Annual Meeting

    Anti-SSA/Ro Mediated Injury to the Endothelium Via Urokinase Plasminogen Activator Receptor/Tgfbeta Activation: Implications in the Pathogenesis of Congenital Heart Block

    Paraskevi Briasouli1, Mark Halushka2, Jill P. Buyon3 and Robert M. Clancy4, 1Rheumatology, New York University Medical Center, New York, NY, 2Division of Cardiovascular Pathology, John Hopkins Pathology, Baltimore, MD, 3Department of Medicine, Division of Rheumatology, New York University School of Medicine, New York, NY, 4Medicine, New York University School of Medicine, New York, NY

    Background/Purpose: One mechanism by which anti-Ro antibodies are linked to the pathogenesis of (cardiac-NL) neonatal lupus is the increased urokinase plasminogen activator (uPA)/urokinase-type plasminogen activator receptor…
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All abstracts accepted to ACR Convergence are under media embargo once the ACR has notified presenters of their abstract’s acceptance. They may be presented at other meetings or published as manuscripts after this time but should not be discussed in non-scholarly venues or outlets. The following embargo policies are strictly enforced by the ACR.

Accepted abstracts are made available to the public online in advance of the meeting and are published in a special online supplement of our scientific journal, Arthritis & Rheumatology. Information contained in those abstracts may not be released until the abstracts appear online. In an exception to the media embargo, academic institutions, private organizations, and companies with products whose value may be influenced by information contained in an abstract may issue a press release to coincide with the availability of an ACR abstract on the ACR website. However, the ACR continues to require that information that goes beyond that contained in the abstract (e.g., discussion of the abstract done as part of editorial news coverage) is under media embargo until 10:00 AM ET on November 14, 2024. Journalists with access to embargoed information cannot release articles or editorial news coverage before this time. Editorial news coverage is considered original articles/videos developed by employed journalists to report facts, commentary, and subject matter expert quotes in a narrative form using a variety of sources (e.g., research, announcements, press releases, events, etc.).

Violation of this policy may result in the abstract being withdrawn from the meeting and other measures deemed appropriate. Authors are responsible for notifying colleagues, institutions, communications firms, and all other stakeholders related to the development or promotion of the abstract about this policy. If you have questions about the ACR abstract embargo policy, please contact ACR abstracts staff at [email protected].

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Accepted abstracts are made available to the public online in advance of the meeting and are published in a special online supplement of Arthritis & Rheumatology. Information contained in those abstracts may not be released until the abstracts appear online. Academic institutions, private organizations and companies with products whose value may be influenced by information contained in an abstract may issue a press release to coincide with the availability of an ACR abstract on the ACR website. However, the ACR continues to require that information that goes beyond that contained in the abstract (e.g., discussion of the abstract done as part a scientific presentation or presentation of additional new information that will be available at the time of the meeting) is under embargo until Saturday, November 11, 2023.

Violation of this policy may result in the abstract being withdrawn from the meeting and other measures deemed appropriate. Authors are responsible for notifying financial and other sponsors about this policy. If you have questions about the abstract embargo policy, please contact the public relations department at [email protected].

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