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. 2017 Jun 1;12(6):e0178748. doi: 10.1371/journal.pone.0178748

Fig 2. CAV1 depletion aggravates fat accumulation in L02 cells and AML12 cells induced by FFA.

Fig 2

CAV1 expression was inhibited using siRNA in L02 cells and stably depleted by applying the CRISPR-Cas9 system by adenovirus recombination in AML12 cells. (A-C) L02 hepatocytes were transfected with scrambled siRNA (NC) or siRNA targeting CAV1 (siCAV1). After transfection for 24 h, cells were challenged with 1 mM FFA for another 48 h. (A) CAV1 mRNA and protein levels in FFA-treated L02 cells transfected with NC or siCAV1. (B) Representative Oil Red O staining of FFA-induced L02 cells with or without CAV1 siRNA transfection. (Original magnification × 400) The average integrated optical density (IOD) of lipid droplets stained with Oil Red O from FFA treated cells was measured with an Image-Pro Plus software. (C) Triglycerides were quantified in L02 cells treated with or without FFA transfected with NC or siCAV1. (D-E) AML12 hepatocytes were transfected with the adenovirus-CRISPR-Cas9 system to stably knockdown CAV1 (CAV1-KD); Ad-NC served as a control. Cells were challenged with 1 mM FFA for 48 h. (D) CAV1 protein levels in FFA-treated AML12 hepatocytes transfected with Ad-NC and CAV1-KD. (E) Triglycerides were quantified from AML12 cells treated with or without FFA transfected with Ad-NC and CAV1-KD. The results are expressed as the mean ± SD of 3 independent experiments. (*P < 0.05, **P < 0.01, and ***P < 0.001).