Fig. 3: Inhibition of DUSP6 in BMMs accelerated the osteoclast differentiation in vitro. | Cell Death & Disease

Fig. 3: Inhibition of DUSP6 in BMMs accelerated the osteoclast differentiation in vitro.

From: DUSP6 expression is associated with osteoporosis through the regulation of osteoclast differentiation via ERK2/Smad2 signaling

Fig. 3

A RANKL-induced osteoclast differentiation was established. We silenced DUSP6 using small interfering RNA (RNAi, #1) or DUSP6 inhibitor (E/Z)-BCI (1 μM). TRAP staining was carried out to explore the differentiation of osteoclast. Original scale bars: 200 μm. B TRAP-positive cells number in per well and relative osteoclast cells were quantitative analyzed. C Bone resorption analysis was used to explore the effect of RNAi or (E/Z)-BCI on the function of osteoclasts. Original scale bars: 200 μm. D F-actin ring formation was carried out between the siControl(siCtrl), siDUSP6(si#1), DMSO and (E/Z)-BCI groups. The actin rings were detected using phalloidin with fluorescence microscopy. The fluorescence intensity was calculated using Imagej. Original scale bars: 200 μm. Quantitative analysis of bone resorption analysis (E) and F-actin ring formation (F). G The osteoclast-related gene expression of NFATc1, C-FOS, ACP5, and DC-STAMP was analyzed (day 5) using real-time PCR in the control and (E/Z)-BCI-treated group. Data in all bar graphs are expressed as mean ± SD (n = 3). *P < 0.05, #P < 0.01.

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