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Fig. 4 | Cell Communication and Signaling

Fig. 4

From: The PPAR-γ antagonist T007 inhibits RANKL-induced osteoclastogenesis and counteracts OVX-induced bone loss in mice

Fig. 4

PPARγ overexpression effectively promoted the RANKL-mediated induction of osteoclast genes and osteoclast differentiation in vitro. a Expression of the osteoclast-specific genes NFATc1, c-Fos, DC-STAMP, Acp5, Atp6v0d2, and CTSK in RAW264.7 cells following the transfection with pcDNA-PPAR γ or the empty vector. b, c The effects of pcDNA-PPARγ or the empty vector on the bone resorption pits were detected using scanning electron microscope (SEM) images, and the resorption pit area measurements by using Image J. d, e The number and areas of TRAP-positive BMMs after the transfection with pcDNA-PPARγ or the empty vector. Untreated cells were used as a control. f RAW264.7 cells were transfected with pcDNA-PPARγ or the empty vector, untreated cells were used as a control. Cell lysates were analyzed using western blotting. The expression of PPARγ, NFATc1, and c-Fos was evaluated. g The effect of PPARγ overexpression on the formation of F-actin ring. All experiments were performed at least three times. *P < 0.05 and **P < 0.01 compared with the control group

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