The cation channel Trpv2 is a new suppressor of arthritis severity, joint damage, and synovial fibroblast invasion.

Authors: Laragione, T  Cheng, KF  Tanner, MR  He, M  Beeton, C  Al-Abed, Y  Gulko, PS 
Citation: Laragione T, etal., Clin Immunol. 2015 Apr 11. pii: S1521-6616(15)00131-X. doi: 10.1016/j.clim.2015.04.001.
Pubmed: (View Article at PubMed) PMID:25869297
DOI: Full-text: DOI:10.1016/j.clim.2015.04.001

Little is known about the regulation of arthritis severity and joint damage in rheumatoid arthritis (RA). Fibroblast-like synoviocytes (FLSs) have a central role in joint damage and express increased levels of the cation channel Trpv2. We aimed at determining the role of Trpv2 in arthritis. Treatment with Trpv2-specific agonists decreased the in vitro invasiveness of FLS from RA patients and arthritic rats and mice. Trpv2 stimulation suppressed IL-1beta-induced expression of MMP-2 and MMP-3. Trpv2 agonists, including the new and more potent LER13, significantly reduced disease severity in KRN serum- and collagen-induced arthritis, and reduced histologic joint damage, synovial inflammation, and synovial blood vessel numbers suggesting anti-angiogenic activity. In this first in vivo use of Trpv2 agonists we discovered a new central role for Trpv2 in arthritis. These new compounds have the potential to become new therapies for RA and other diseases associated with inflammation, invasion, and angiogenesis.

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CRRD Object Information
CRRD ID: 9999444
Created: 2015-04-21
Species: All species
Last Modified: 2015-04-21
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.