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Protein, Receptor May Play Role in Rheumatoid Inflammation

Placenta growth factor and flt-1 spur production of proinflammatory cytokines in rheumatoid arthritis

WEDNESDAY, Feb. 11 (HealthDay News) -- Placenta growth factor (PlGF) may promote inflammation and angiogenesis in joints in patients with rheumatoid arthritis, but not healthy joints, according to research published in the February issue of Arthritis & Rheumatism.

Seung-Ah Yoo, of the Catholic University of Korea in Seoul, South Korea, and colleagues found that PlGF was constitutively expressed in fibroblast-like synoviocytes in patients with rheumatoid arthritis, and production rose up to 3.2-fold when cells were stimulated with IL-1β. PlGF appeared to spur monocytes and macrophages to create TNFα and IL-6.

The authors write that high-level expression of flt-1 -- a specific PlGF receptor -- associated with inflammatory responses may cause the PlGF-induced increases in TNFα and IL-6 production seen in individuals with rheumatoid arthritis. In mice that underwent induced arthritis, the use of an anti-flt-1 peptide was associated with decreased arthritis due to inhibited production of IL-6 and anti-type II collagen antibody, the researchers report.

"Use of an anti-flt-1 peptide may be an effective strategy in the treatment of chronic inflammatory arthritis, through suppression of the PlGF-stimulated production of TNFα and IL-6. These findings provide new insight into the pathogenic mechanism of rheumatoid arthritis and emphasize the importance of PlGF and flt-1 as potential candidates for therapy, in addition to their being a common cue of angiogenesis and the inflammatory process," the authors conclude.

A study co-author is a co-inventor on a patent for inhibitors of PlGF/flt-1 interaction.

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