ACR Meeting Abstracts

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Abstracts tagged "Fibroblasts"

  • Abstract Number: 973 • 2017 ACR/ARHP Annual Meeting

    IL-6 and TNF-a Cooperate to Modulate the Cell Cycle of RA-Fibroblast-like Synoviocytes Via Cyclin Dependent Kinase Inhibitors

    Kenta Kaneshiro1, Kohsuke Yoshida1, Ayako Nakai1, Kohjin Suzuki1, Koto Uchida1, Teppei Hashimoto2, Yoshiko Kawasaki3, Natsuko Nakagawa4, Koji Tateishi5, Nao Shibanuma6, Yoshitada Sakai7 and Akira Hashiramoto1, 1Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan, 2Department of Rheumatology, Kobe Kaisei Hospital, Kobe, Japan, 3The Center of Rheumatic Diseases, Department of Rheumatology, Kobe Kaisei Hospital, Kobe, Japan, 4Department of Orthopaedic Surgery, Konan-Kakogawa Hospital, Kakogawa, Japan, 5Orthpaedic Surgery, Kobe University Graduate School of Medicine, Kobe, Japan, 6Departmant of Orthopaedic Surgery, Kobe Kaisei Hospital, Kobe, Japan, 7Division of Rehabilitation Medicine, Kobe University Graduate School of Medicine, Kobe, Japan

    Background/Purpose: IL-6 and TNF-α play an important role in the pathogenesis of RA, and the proliferation of RA-synoviocytes (FLS) is controlled by cell cycle regulators…
  • Abstract Number: 974 • 2017 ACR/ARHP Annual Meeting

    Leucine-Rich α-2 Glycoprotein Promotes Lung Fibrosis By Modulating TGF-β Signaling in Fibroblasts

    Hiromi Honda, Minoru Fujimoto, Satoshi Serada, Hyun Lee, Tomoharu Ohkawara and Tetsuji Naka, Center for Intractable Immune Disease, Kochi University, Nankoku, Japan

    Background/Purpose: Interstitial lung disease (ILD) is one of the most common extraarticular manifestation of rheumatoid arthritis. ILD is characterized by progressive fibrosis of the lung…
  • Abstract Number: 975 • 2017 ACR/ARHP Annual Meeting

    IL-17A Induced Autophagy That the Proliferation of Rheumatoid Arthritis Fibroblast-like Synoviocytes through Down-Regulation of PI3K/AKT/mTOR Signaling Pathway

    Sang-Hyon Kim1, Jihye Bang2, Ji-Min Kim1, Chang-Nam Son1, Jin-Nyeong Chae1 and Hye-Jin Jeong3, 1Division of Rheumatology, Department of Internal Medicine, Keimyung University Dongsan Medical Center, Keimyung University School of Medicine, Daegu, Republic of Korea, Daegu, Korea, Republic of (South), 2Division of Rheumatology, Department of Internal Medicine, Dongsan Medical Center, Keimyung University School of Medicine, Daegu, Korea, Republic of (South), 3Department of Rheumatology, Keimyung University Dongsan Medical Center, Daegu, Korea, Republic of (South)

    Background/Purpose: Autophagy is generally thought of as a survival mechanism, although its deregulation has been linked to non-apoptotic cell death. Fibroblast-like synoviocytes (FLS) resistance to…
  • Abstract Number: 1409 • 2017 ACR/ARHP Annual Meeting

    Ursolic Acid Promotes Apoptosis of Rheumatoid Athritis Synovial Fibroblasts By Upregulating Noxa Expression and Recruiting E3 Ligase Mule to Degrade Mcl-1

    Eugene Kim1, Solomon Agere1, Sadik Khuder2 and Salahuddin Ahmed1, 1Department of Pharmaceutical Sciences, Washington State University, College of Pharmacy, Spokane, WA, 2Department of Medicine, University of Toledo, Toledo, OH

    Background/Purpose: In our previous study, we discovered that ursolic acid (UA), a pentacyclic triterpenoid with anti-inflammatory properties, induces apoptosis in synovial fibroblasts from rheumatoid arthritis…
  • Abstract Number: 1415 • 2017 ACR/ARHP Annual Meeting

    TNF-Induced IRF1 Is Critical for the Inflammatory Gene Expression in Fibroblast-like Synoviocytes

    Michael Bonelli1, Karolina von Dalwigk2, Birgit Niederreiter1, Thomas Pap3, Josef S. Smolen4, Hans Peter Kiener1 and Thomas Karonitsch1, 1Rheumatology, Medical University of Vienna, Vienna, Austria, 2Department of Rheumatology, Medical University of Vienna, Vienna, Austria, 3Institute of Musculoskeletal Medicine, University Hospital Muenster, Muenster, Germany, 4Medical University Vienna, Division of Rheumatology, Department of Internal Medicine III, Vienna, Austria

    Background/Purpose: Fibroblast-like synoviocytes (FLS) are increasingly recognised as major pathogenic cells in synovial inflammation of patients with Rheumatoid Arthritis (RA). In response to pro-inflammatory stimuli,…
  • Abstract Number: 1417 • 2017 ACR/ARHP Annual Meeting

    Mitophagy Defect in Fibroblast-like Synoviocytes of Rheumatoid Arthritis Is Improved By Pyruvate Treatment

    Jeong Yeon Kim1,2, ShinEui Kang3,4, Hyun Jung Yoo1,5, Ji Soo Park1,2, Sehui Shon1,2, Eun Young Lee2, Eun Bong Lee5 and Yeong Wook Song1,6, 1Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, Korea., Seoul, Korea, Republic of (South), 2Division of Rheumatology, Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea., Seoul, Korea, Republic of (South), 3Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul, Korea., seoul, Korea, Republic of (South), 4Division of Rheumatology, Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea., seoul, Korea, Republic of (South), 5Division of Rheumatology, Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea, Republic of (South), 6Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, and College of Medicine, Seoul National University, Seoul, Korea, Republic of (South)

    Background/Purpose: Fibroblast-like synoviocytes (FLS) in the synovial intimal lining produce pro-inflammatory cytokines resulting in increase of joint inflammation. Recent studies about the cellular metabolism in…
  • Abstract Number: 171 • 2017 ACR/ARHP Annual Meeting

    Finding Transcriptional Regulators Central to RA with Transcriptomics of IL17 Dose Response, Time Series, and siRNA Silencing in Stromal Cells

    Kamil Slowikowski1, Hung Nguyen2, Gerald Watts2, Fumitaka Mizoguchi3, Erika H. Noss4, Michael Brenner5 and Soumya Raychaudhuri6, 1Harvard University, Boston, MA, 2Brigham and Women's Hospital, Boston, MA, 3Department of Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan, 4Division of Rheumatology, University of Washington, Seattle, WA, 5Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 6Division of Medicine and Rheumatology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA

    Background/Purpose: Rheumatoid arthritis (RA) is characterized by immune cell infiltration into the synovial membrane of the joint, where they engage stromal cells such as synovial…
  • Abstract Number: 1714 • 2017 ACR/ARHP Annual Meeting

    Inhibition of Hedgehog Acyltransferase Alleviates the Profibrotic Effects of Transforming Growth Factor β in Systemic Sclerosis

    Ruifang Liang1, Rosebeth Kagwiria2, Clara Dees3, Yun Zhang4, Oliver Distler5, Georg Schett6 and Jörg Distler7, 1Department of Internal Medicine 3 – Rheumatology and Immunology, Universitätsklinikum Erlangen, Department of Internal Medicine 3 and Institute for Clinical Immunology, Friedrich-Alexander-University of Erlangen-Nuremberg and University Hospital Erlangen, Erlangen, Germany, 2Department of Internal Medicine 3 and Institute for Clinical Immunology, Friedrich-Alexander-University of Erlangen-Nuremberg and University Hospital Erlangen, Erlangen, Germany, 3Department of Internal Medicine 3 and Institute for Clinical Immunology,, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany, 4Department of Internal Medicine 3 and Institute for Clinical Immunology, Department of Internal Medicine 3 and Institute for Clinical Immunology, Friedrich-Alexander-University of Erlangen-Nuremberg and University Hospital Erlangen, Erlangen, Germany, 5Department of Rheumatology, University Hospital Zurich, Zurich, Switzerland, 6Department of Internal Medicine 3 – Rheumatology and Immunology, Department of Internal Medicine 3 and Institute for Clinical Immunology, Friedrich-Alexander-University of Erlangen-Nuremberg and University Hospital Erlangen, Erlangen, Germany, 7Department of Internal Medicine 3 – Rheumatology and Immunology, Universitätsklinikum Erlangen, Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany

    Background/Purpose: Hedgehog acyltransferase (Hhat) catalyzes the attachment of the fatty acid palmitate onto Sonic Hedgehog (Shh), a modification essential for Shh signaling activity. Palmitoylation of…
  • Abstract Number: 1661 • 2016 ACR/ARHP Annual Meeting

    Toll-like Receptor 4 Induced IL-20 and IL-24 Stimulate Osteoblast Mineralization and Are Increased in Spondyloarthritis

    Tue Wenzel Kragstrup1,2, Morten Nørgaard Andersen3, Berit Schiøttz-Christensen4, Anne Grethe Jurik5, Malene Hvid6 and Bent Deleuran1, 1Department of Biomedicine, Aarhus University, Aarhus, Denmark, 2Department of Rheumatology, Aarhus University Hospital, Aarhus, Denmark, 3Aarhus University, Aarhus, Denmark, 4Hospital Lillebaelt, Middelfart, Denmark, 5Aarhus University Hospital, Aarhus, Denmark, 6Department of Clinical Medicine, Aarhus University, Aarhus, Denmark

    Background/Purpose: The pathogenesis of spondyloarthritis (SpA) involves activation of the innate immune system, inflammation and new bone formation. The innate immune system is activated through…
  • Abstract Number: 1671 • 2016 ACR/ARHP Annual Meeting

    Pirfenidone Might Inhibit New Bone Formation in Spondyloarthritis: Proof of Concept Study Using Cell Culture Models

    Julie Laustsen1, Søren Lomholt1, Pernille Andersen2, Jens Kelsen3 and Tue Wenzel Kragstrup1,4, 1Department of Biomedicine, Aarhus University, Aarhus, Denmark, 2Interdisciplinary Nanoscience Center, Aarhus University, Aarhus, Denmark, 3Department of Gastroenterology, Aarhus University Hospital, Aarhus, Denmark, 4Department of Rheumatology, Aarhus University Hospital, Aarhus, Denmark

    Background/Purpose:  The pathogenesis of spondyloarthritis (SpA) involves both inflammation and new bone formation in the spine. In line with this, the disease has been characterized…
  • Abstract Number: 1852 • 2016 ACR/ARHP Annual Meeting

    Decreased Expression of Sirtuin 7 By Lung Fibroblasts from Patients with Scleroderma Contributes to Elevated Collagen Production

    Anne E. Wyman1,2, Zahid Noor1, Nevins W. Todd1,2, Irina G. Luzina1,2 and Sergei P. Atamas1,2, 1University of Maryland School of Medicine, Baltimore, MD, 2Baltimore VA Medical Center, Baltimore, MD

    Background/Purpose:  Pulmonary fibrosis is a severe complication of systemic sclerosis (SSc). Changes in the expression levels of sirtuins (SIRTs), a family of NAD+-dependent histone deacetylases,…
  • Abstract Number: 1855 • 2016 ACR/ARHP Annual Meeting

    Phosphodiesterase-5 Inhibitors Attenuate Fibrotic Phenotype and Restore Anti-Fibrotic Resopnses of Cutaneous Fibroblasts in Patients with Scleroderma

    Vikas Agarwal1, Mohit kumar Rai1, Vinita Agrawal2, Harshit Singh1 and Saurabh Chaturvedi1, 1Clinical Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India, 2Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Lucknow, India

    Background/Purpose:  Scleroderma (SSc) is a chronic autoimmune disease, characterized by excessive fibrosis of skin and internal organs due to uncontrolled proliferation of fibroblasts and deposition…
  • Abstract Number: 1857 • 2016 ACR/ARHP Annual Meeting

    A Novel Highly Selective 5-Hydroxytryptamine 2B (5-HT2B) Receptor Antagonist Ameliorating Fibrosis in Preclinical Models of Systemic Sclerosis

    Christina Wenglén1, Lars Pettersson2, Helena Arozenius2 and Gunilla Ekström1, 1R&D, AnaMar AB, Lund, Sweden, 2AnaMar AB, Lund, Sweden

    Background/Purpose:   Methods:   Results:   Conclusion: The results demonstrate that the 5-HT2B receptor antagonist AM1125 prevents pro-fibrotic events in human dermal fibroblasts and attenuates…
  • Abstract Number: 2071 • 2016 ACR/ARHP Annual Meeting

    Expression of Neuraminidase 1 (NEU1) Is Upregulated in the Lungs of Scleroderma Patients with Pulmonary Fibrosis, and Gene Delivery of NEU1 to Mouse Lungs Elicits Accumulation of CD8+ Lymphocytes and Collagen

    Irina G. Luzina1,2, Anne E. Wyman1,2, Virginia Lockatell2, Zahid Noor2, Nevins W. Todd1,2, Simeon E. Goldblum1,2 and Sergei P. Atamas1,2, 1Baltimore VA Medical Center, Baltimore, MD, 2University of Maryland School of Medicine, Baltimore, MD

    Background/Purpose:  We and others have previously reported that pulmonary fibrosis in patients with scleroderma is accompanied by pulmonary accumulation of predominantly CD8+ T lymphocytes. Earlier…
  • Abstract Number: 2072 • 2016 ACR/ARHP Annual Meeting

    Fli1-Haploinsufficient Dermal Fibroblasts Promote Skin-Localized Transdifferentiation of Th2- and Th17-like Regulatory T Cells

    Ryosuke Saigusa1, Yoshihide Asano2, Takuya Miyagawa2, Megumi Hirabayashi2, Kouki Nakamura1, Shunsuke Miura3, Takashi Yamashita2, Yohei Ichimura1, Takehiro Takahashi1, Tetsuo Toyama2, Takashi Taniguchi1, Ayumi Yoshizaki2, Maria Trojanowska4 and Shinichi Sato1, 1Dermatology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan, 2Dermatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan, 3University of Tokyo Graduate School of Medicine, Tokyo, Japan, 4Arthritis Center, Boston University, Arthritis Center, Boston, MA

    Background/Purpose:  Systemic sclerosis (SSc) is a multisystem connective tissue disease characterized by autoimmunity/inflammation, vasculopathy, and tissue fibrosis. Fli1 is a member of Ets family transcription…
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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.).

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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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