The University of Osaka · Medicine
Professor Tetsuya Tomita's research lab focuses on molecular and gene therapy approaches for inflammatory joint diseases, particularly rheumatoid arthritis (RA). The lab investigates transcription factors such as NF-κB and signaling molecules like EMMPRIN and PPARγ to understand their roles in joint inflammation and destruction. Key research directions include the development of gene therapy strategies using decoy oligodeoxynucleotides (ODNs) and small molecule agonists to modulate inflammatory pathways and protect joint integrity. The lab also explores direct gene transfer techniques for sustained therapeutic protein expression in target tissues.
Figures are computed from collected data and may differ slightly.
The present results demonstrate that administration of NF-kappaB decoy ODN in arthritic joints of rats with CIA led to an amelioration of arthritis. These findings suggest that intraarticular transfection of NF-kappaB decoy ODN may provide a useful therapeutic approach for the treatment of inflammatory arthritis.
Myelography was performed in 535 patients at the Memorial Sloan-Kettering Hospital from January 1979 to December 1979. In 110 cases a complete block was demonstrated and of these, 78 had epidural metastases. A uniform treatment was applied using radiation therapy and high dose steroid. The neurologic outcome for each patient was evaluated, correlating pre-treatment neurologic status, pathologic type, nature of block (level, structural versus tumoral), and result of repeat fluoromyelography. Only
The results demonstrated in this study suggest the potential usefulness of NFkappaB decoy ODN for gene therapy of inflammatory synovitis of RA.
The transfection frequency and stability of expression recognized in this study indicate the possibility of a strategy for treatment of joint disorders, including arthritis, using direct gene transfer.
The expression of EMMPRIN stimulates the production of MMP-1 and MMP-3 in the synovial tissue of affected joints in RA. The results of this study suggest that EMMPRIN may be one of the important factors in progressive joint destruction in RA.
THR0921 is a novel peroxisome proliferator-activated receptor gamma (PPARgamma) agonist with potent anti-diabetic properties. Because of the proposed role of PPARgamma in inflammation, we investigated the potential of orally active THR0921 to inhibit the pathogenesis of collagen-induced arthritis (CIA). CIA was induced in DBA/1J mice by the injection of bovine type II collagen in complete Freund's adjuvant on days 0 and 21. Mice were treated with THR0921 (50 mg/kg/day) starting on the day of the
Open papers in the app to read, cite, and organize with AI.
