Regulation of DREAM Expression by Group I mGluR

DREAM (downstream regulatory element antagonistic modulator) is a calcium-binding protein that regulates dynorphin expression, promotes potassium channel surface expression, and enhances presenilin processing in an expression level-dependent manner. However, no molecular mechanism has yet explained how protein levels of DREAM are regulated. Here we identified group I mGluR (mGluR1/5) as a positive regulator of DREAM protein expression. Overexpression of mGluR1/5 increased the cellular level of DREAM. Up-regulation of DREAM resulted in increased DREAM protein in both the nucleus and cytoplasm, where the protein acts as a transcriptional repressor and a modulator of its interacting proteins, respectively. DHPG (3,5-dihydroxyphenylglycine), a group I mGluR agonist, also up-regulated DREAM expression in cortical neurons. These results suggest that group I mGluR is the first identified receptor that may regulate DREAM activity in neurons.

A Case of Peritoneal Tuberculosis with Poncet's Disease in a Patient Treated with Infliximab

Infliximab is a chimeric mouse/human monoclonal antibody against tumor necrosis factor-alpha (TNF-alpha) that is used worldwide to treat rheumatic disease. However, the reactivation of tuberculosis, including extrapulmonary menifestation, is a severe side effect of anti-TNF-alpha treatment. Mycobacterium tubercluosis causes two forms of joint involvement, TB arthritis and Poncet's disease. Poncet's disease is a rare aseptic form of arthritis, known as reactive arthritis in tuberculosis. We encountered a case of tuberculous peritonitis with Poncet's disease in a 38-yearold man with a history of ankylosing spondylitis that was treated with infliximab. We report this case with a review of the literature.

Inhibition of Fas-mediated Apoptosis of Rheumatoid Synovial Cells by TGF-beta and IL-1 beta / 대한류마티스학회지

OBJECTIVE: To investigate the proliferative and anti-apoptotic effects of TGF-beta and IL-1beta on rheumatoid synovial cells. METHODS: Synovial cells obtained from surgical procedure of the rheumatoid joint were cultured with TFG-beta and IL-1beta The proliferative response of synovial cells was examined by non-radioactive cell proliferation assay. Fas-demiated apoptosis of synovial cells was measured by flow cytometry after addition of anti-Fas antibody. RESULTS: TGF-beta and IL-1betaproliferated synovial cells in a dose-dependent manner. They also made synovial cells resistant to anti-Fas antibody induced apoptosis. CONCLUSION: TGF-beta and IL-1betapromotes synovial cell proliferation possibly through interference with Fas-mediated apoptosis, suggesting their role in synovial hyperplasis in rheumatoid arthritis.