Fig. 4: RANKL treatment increases PRMT1 expression via JNK-dependent signaling in osteoclast differentiation.
From: PRMT1 mediates RANKL-induced osteoclastogenesis and contributes to bone loss in ovariectomized mice
a BMDMs were stimulated by RANKL (100 ng/ml) at the indicated time points and were subjected to western blotting with the indicated antibodies. b-d The BMDMs were pre-treated with DMSO (Veh), SB 203580 (SB, 10 μM), SP 600125 (SP, 10 μM) or PD 98059 (PD, 10 μM) in the presence of M-CSF (30 ng/ml). After 30 min, the cells were stimulated with RANKL (100 ng/ml) for 24 h. b PRMT1 protein expression was examined via western blotting and c its mRNA level was measured with a real-time PCR analysis normalized to the β-actin level. The results are expressed as the mean ± SD. **p < 0.01, ***p < 0.001. d The cells were labeled with anti-PRMT1 and fluorescein isothiocyanate (FITC)-conjugated secondary antibody, and the nuclei were stained with DAPI and observed under a confocal microscope. Representative images are from at least three independent experiments. Scale bar: 10 μm. e Fluorescence intensities were obtained from the mean value of the selected regions in the image using Leica Application Suite Advanced Fluorescence (LAS AF) software (Leica Microsystems). The results are expressed as the mean ± SD. **p < 0.01, ***p < 0.001
