Regulatory mechanisms of TSG-6 (TNF-alfa-induced protein-6: Tnfip6)-deficient and wild-type synovial fibroblasts

BALB/c mice are susceptible to proteoglycan (PG) aggrecan-induced arthritis (PGIA), and the absence of TSG-6 further increases susceptibility and local inflammatory reactions, including neutrophil invasion into the joints. To gain insight into the mechanisms of TSG-6 action, synovial fibroblasts were isolated from wild-type and TSG-6-KO mice, cultured and exposed to various agents affecting either the TSG-6 expression and/or modify the intracellular function of TSG-6. In the present microarray studies, we have identified differences in gene expression by fibroblasts isolated from wild-type or TSG-6-KO mice Keywords: Genetic modification In this study we compared the gene expression profile of 42 fibroblast cultures from mouse synovial samples. Fifteen samples were wild-type and 27 samples were TSG-6 knockout. In these two genotype groups fibroblasts were treated with TNFa, LPS, TSG-6, HA, or HA+TSG-6, and were compared to untreated samples in the same genotype group. We also compared the same treatments between KO and WT.