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. 2015 Nov 30;13(1):98–108. doi: 10.1080/15476286.2015.1122164

Figure 1.

Figure 1.

ANRIL expression is induced by pro-inflammatory factors in ECs. (A) RT-qPCR analysis of ANRIL expression in HUVECs treated with TNF-α (25 ng/mL), IFN-γ (100 ng/mL), PDGF-BB (10 ng/mL) or VEGF165 (50 ng/mL) for 24 hours. (**p < 0.01, ***p < 0.005, n.s., non-significant vs. control). (B) RT-qPCR showing that ANRIL levels were induced by TNF-α (25 ng/mL) in a time-dependent manner. (**p < 0.01, ***p < 0.005 vs. control). (C) RT-qPCR showing that ANRIL levels were induced by TNF-α (24h) in a dose-dependent manner. (*p < 0.05, **p < 0.01 vs. control). (D and E) Both short (D) and long (E) ANRIL isoforms were upregulated upon TNF-α treatment (25 ng/mL) at indicated time points by RT-qPCR. (**p < 0.01, ***p < 0.005 vs. control). (F) Cell fractionation and RT-qPCR analysis in HUVECs showing that ANRIL was mainly distributed in nucleus upon control or TNF-α (25 ng/mL) treatment. (*p < 0.05). All results are presented as mean ± SEM from at least 3 independent biological experiments.