ACR Meeting Abstracts

ACR Meeting Abstracts

  • Meetings
    • ACR Convergence 2024
    • ACR Convergence 2023
    • 2023 ACR/ARP PRSYM
    • ACR Convergence 2022
    • ACR Convergence 2021
    • ACR Convergence 2020
    • 2020 ACR/ARP PRSYM
    • 2019 ACR/ARP Annual Meeting
    • 2018-2009 Meetings
    • Download Abstracts
  • Keyword Index
  • Advanced Search
  • Your Favorites
    • Favorites
    • Login
    • View and print all favorites
    • Clear all your favorites
  • ACR Meetings

Abstract Number: 1850

The Bromodomain Protein Inhibitor I-BET151 Suppresses Inflammatory and Matrix Degrading Properties Of Rheumatoid Arthritis Synovial Fibroblasts

Kerstin Klein1, Renate E. Gay2, Christoph Kolling3, Lih-Ling Lin4, Steffen Gay1 and Caroline Ospelt1, 1Center of Experimental Rheumatology, University Hospital Zurich and Zurich Center of Integrative Human Physiology (ZIHP), Zurich, Switzerland, 2Center of Experimental Rheumatology, Zurich University Hospital, Zurich, Switzerland, 3Schultess Clinic, Zurich, Switzerland, 4Inflammation and Remodeling Research Unit, Pfizer, Cambridge, MA

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Epigenetics, fibroblasts and inflammation

  • Tweet
  • Click to email a link to a friend (Opens in new window) Email
  • Click to print (Opens in new window) Print
Session Information

Title: Cytokines, Mediators, Cell-cell Adhesion, Cell Trafficking and Angiogenesis II

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Bromodomain proteins (BRD) contain conserved acetyl-lysine binding domains that specifically recognize ε-N-lysine acetylation motifs, a key event in the reading process of epigenetic marks. Recently, a functional role of the BET bromodomain proteins BRD2, BRD3, and BRD4 in inflammation was described and BET inhibitors were shown to inhibit the expression of pro-inflammatory cytokines and chemokines in LPS-stimulated macrophages (Nicodeme et al., Nature. 2010). Our objectives were to evaluate the expression of the BET proteins BRD2, BRD3 and BRD4 in rheumatoid arthritis synovial fibroblasts (RASF) and to investigate the effects of the BET protein inhibitor I-BET151 on expression levels and functional properties of RASF.

Methods:

The mRNA expression levels of BRD2, BRD3 and BRD4 in RASF and osteoarthritis synovial fibroblasts (OASF) were verified by quantitative Real-time PCR.  RASF were treated with the inflammatory cytokines TNF-α (10 ng/ml), IL1β (1 ng/ml) and the Toll-like receptor (TLR) ligands Pam3 (100 ng/ml), pIC (10 µg/ml), and LPS (100 ng/ml) in presence or absence of I-BET151 (1 µM, R&D Systems) for 24h. The mRNA expression levels and secretion rates into cell culture supernatants of MMP1, MMP3, IL6, IL8 and CCL5 were evaluated by quantitative Real-time PCR and ELISA. Rates of proliferation and migratory properties of RASF before and after I-BET151 treatment were investigated using a BrdU-based proliferation assay and scratch assays, respectively.

Results:

BRD2 (delta Ct: OASF: 5.93 ± 0.22; RASF: 5.47 ± 0.47; p<0.01) and BRD3 (delta Ct: OASF: 7.94 ± 0.67; RASF: 7.27 ± 0.56; p<0.01) mRNA levels were slightly increased in RASF (n=20) compared to OASF (n=10). On the other hand, BRD4 mRNA levels were similar in OASF and RASF (delta Ct: OASF: 4.94 ± 0.26; RASF: 4.95 ± 0.36). Treatment of RASF (n=12) with I-BET151 significantly reduced basal IL6 mRNA levels (p<0.001), as well as the mRNA expression levels of IL6, IL8, MMP1, MMP3 and CCL5 after stimulation with cytokines and TLR ligands (p<0.05).  Furthermore, basal IL6 and IL8 secretion rates were decreased after I-BET151 treatment of RASF (n=10-12) by 75.9% (p<0.01) and 39.4% (p<0.01), respectively. Both, IL6 and IL8 secretion rates remained decreased after I-BET151 treatment of RASF (n=9-12, p<0.01) after stimulation with cytokines and TLR ligands between 53.6 and 79%.  Whereas I-BET151 significantly reduced MMP1 secretion rates only after TNF-α (71.5%, p<0.01), IL1β (75.6%, p<0.01) and pIC (32.8%, p<0.05) (n=12), MMP3 levels in supernatants (n=12) were reduced after stimulation with all cytokines and TLR ligands by 29.5–82.2% (p<0.05). CCL5 secretion was reduced in I-BET151 treated RASF (n=6) by 51.3–67.2%, depending on the stimuli. Furthermore, rates of proliferation were reduced by 61.4 ± 14.3 % (p=0.0625) in RASF (n=5) treated with I-BET151, whereas migratory properties of RASF (n=2) were not affected.

Conclusion:

Our results demonstrate that I-BET151 is a strong suppressor of the inflammatory, matrix degrading and proliferating properties of RASF and suggest a therapeutic potential of blocking the recruitment of BET proteins to promoters of target genes in RA.


Disclosure:

K. Klein,
None;

R. E. Gay,
None;

C. Kolling,
None;

L. L. Lin,

Employment,

3;

S. Gay,
None;

C. Ospelt,
None.

  • Tweet
  • Click to email a link to a friend (Opens in new window) Email
  • Click to print (Opens in new window) Print

« Back to 2013 ACR/ARHP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/the-bromodomain-protein-inhibitor-i-bet151-suppresses-inflammatory-and-matrix-degrading-properties-of-rheumatoid-arthritis-synovial-fibroblasts/

Advanced Search

Your Favorites

You can save and print a list of your favorite abstracts during your browser session by clicking the “Favorite” button at the bottom of any abstract. View your favorites »

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].

Wiley

  • Online Journal
  • Privacy Policy
  • Permissions Policies
  • Cookie Preferences

© Copyright 2025 American College of Rheumatology