Fig. 5
Ang II increased NFATC1 expression in synovial cells via the RANKL pathway. Synovial cells were pretreated with or without the AT1R antagonist (olmesartan, Olm, 10−5 M), the AT2R antagonist (PD123319, PD, 10−5 M), the ERK1/2 inhibitor (U0126, 5×10−6 M), the JNK inhibitor (SP600125, SP 1×10−5 M), or the p38MAPK inhibitor (SB203580, SB, 10−5 M) for 30 min, or transfected with control or RANKL-specific siRNA for 48 h, and then exposed to Ang II (10−6 M) for 48 h. The relative mRNA and protein levels of RANKL and NFATC1 in different groups were evaluated by RT-PCR and western-blot. Data are representative images or expressed as the mean ± SD of three independent experiments with synovial cells from each RA patient. a The relative level of RANKL mRNA transcripts was determined by RT-PCR (n = 3). b RT-PCR analysis of NFATC1 expression (n = 3). c Western blot analysis of NFATC1 expression (n = 3). *p < 0.01 vs. the control group; #p < 0.01 vs. the Ang II group