Referenced in: none

Automatically associated channels: TRP , TRPV , TRPV2

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

Authors: Teresina Laragione, Kai F Cheng, Mark R Tanner, Mingzhu He, Christine Beeton, Yousef Al-Abed, Pércio S Gulko

Journal, date & volume: Clin. Immunol., 2015 Apr 10 , ,

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/25869297

Abstract
Little is known about the regulation of arthritis severity and joint damage in rheumatoid arthritis (RA). Fibroblast-like synoviocytes (FLS) 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-1β-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.