system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Apoptosis, Arthritis, Rheumatoid, Cell Survival, Cells, Cultured, Cyclin-Dependent Kinase Inhibitor p21, Dose-Response Relationship, Drug, Drug Combinations, Drug Synergism, Enzyme Inhibitors, Fibroblasts, Flow Cytometry, Fluorescent Antibody Technique, Indirect, Humans, Hydroxamic Acids, RNA, Messenger, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, Synovial Membrane, fas Receptor.
user
Does trichostatin A cooperate with Fas-mediated signal to induce apoptosis in rheumatoid arthritis synovial fibroblasts? Context: To clarify the effects of trichostatin A (TSA), a histone deacetylase inhibitor, on the growth and survival of rheumatoid arthritis synovial fibroblasts (RA-SF). Cell viability was assessed using a WST-8 assay and direct cell counting. Apoptosis was detected by annexin V staining on a flow cytometer. Protein and mRNA expression was determined by Western blotting, flow cytometry, and RT-PCR. TSA suppressed cell growth of RA-SF in a dose-dependent manner, as determined by WST-8 assay and direct cell counting. Other histone deacetylase inhibitors also showed inhibitory effects on RA-SF proliferation. TSA upregulated p21(WAF1/CIP1) cell cycle inhibitor, suggesting that cell cycle arrest is involved in the reduction of cell numbers. In addition, TSA cooperated with Fas-induced pathway to induce cell death, determined by WST-8 assay and annexin V staining. TSA reduced FLICE inhibitory protein (FLIP) expression but not Bcl-2, Bcl-XL, and Fas expression, indicating that the synergistic effect may be through downregulation of FLIP.
assistant
TSA has antirheumatic effects on RA-SF and might be a potential therapeutic tool for the treatment of RA. Final Decision: yes