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Figure 7 IL-6 and COX-2 expression levels after miRNA modulation and IL-1β stimulation. Quan- titative real-time PCR of IL-6 (A-C and G-I) and COX-2 (D-F and J-L) expression in human fetal astrocytes (A-F) and SEGA-derived cell cultures (G-L) after transfection with either mimic or inhibitor of miR21 (A, D, G, J), miR146a (B, E, H, K) and miR155 (C, F, I, L). Data are expressed rela- tive to the levels observed in untreated cells and are mean ± SEM from five fetal and four SEGA experiments on cultures derived from separate donors performed in duplicate. *p<0.05, **p<0.01, ***p<0.001 compared to control; #p<0.05, ##p<0.01, ###p<0.001 between experimental sam- ples, Mann Whitney U test. SEGA: subependymal giant cell astrocytomas.
miR146a to modulate the IL-1R/TLR pathway, targeting downstream signaling molecules; 26, 36-38. In both human astrocytes and SEGA cell cultures transfection with miR146a mimic reduced IRAK1 and TRAF6 mRNA after stimulation with IL-1β and modulation of IRAK2 was also detected in SEGA cells. Another potential target of both miR146a and miR155 is complement factor H (CFH), which is a major negative regulator of the innate immune and inflammatory response 79, 80. Thus, the possible repression of CFH, has to be taken into account with respect to the interpretation of the ultimate effects of changes in the expression of miR146a. However, under our experimental conditions and in both cell types used, we did not detect significant changes in the expression of CFH after overex-