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. Author manuscript; available in PMC: 2018 Aug 15.
Published in final edited form as: Toxicol Appl Pharmacol. 2017 May 17;329:48–57. doi: 10.1016/j.taap.2017.05.019

Figure 4.

Figure 4

Butylparaben activates PPARγ, but not a GR responsive reporter, in C3H10T1/2 cells. (A) C3H10T1/2 cells were seeded and transiently transfected with PPARγ transactivation reporters (Left panel) or MMTV-Luc (Right panel) and β-gal control plasmid for 24 h and treated with or without methyl- (100 μM), butylparaben (100 μM), DMSO, Rosi (1 μM) or Dex (1 μM) as indicated for 18 h before the cells were lysed and reporter activities were measured. Relative luciferase activities are luciferase activities normalized by β-gal activities and are expressed as fold of the negative control (−) (set at 1). (B) C3H10T1/2 cells were stably infected with lentiviral shRNA particles targeting against GR, PPARγ, or a scrambled control (SCR). Knockdown (KD) efficiency was determined by western analysis (Left panel) and quantified by densitometry (Right panels). (C) C3H10T1/2 cells with stable knockdown of PPARγ (PPARγ KD), GR (GR KD), or the scrambled controls (SCR) were seeded and transiently transfected with PPARγ transactivation reporters (Left panels) or MMTV-Luc (Right panels) and β-gal control plasmid for 24 h and treated with or without methyl- (100 μM), butylparaben (100 μM), DMSO, Rosi (1 μM) or Dex (1 μM) for 18 h before the cells were lysed and reporter activities were measured. Relative luciferase activities are luciferase activities normalized by β-gal activities and are expressed as fold of the negative control (−) (set at 1). Data are mean ± SEM (n=3). *, ***, p<0.05 and p<0.01 versus DMSO, respectively.