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. 2021 Mar 3;42(12):2106–2119. doi: 10.1038/s41401-021-00617-4

Fig. 5. KLF5 was transcriptionally regulated by the HIF-1α C-TAD.

Fig. 5

a KLF5 expression was analyzed in primary TECs with simulated severe I/RI after FIH-1 was overexpressed with adenovirus (Ad-FIH-1). Scale bars, 20 μm. b Luciferase reporter assays were performed using constructs with HIF-1α or HIF-1α C-TAD KO. 293T cells were transfected with these constructs along with the HRE-KLF5-Luc overexpression plasmid. Data were obtained from four independent experiments. **P < 0.01 versus the HIF-1α-NC (pcDNA3 empty vector) + HRE-KLF5-Luc group; #P < 0.01 versus the HIF-1α+KLF5-Luc group (Bonferroni correction, two comparisons were made). c The HIF-1α N-TAD+C-TAD-Gal4, HIF-1α N-TAD-Gal4, or HIF-1α C-TAD-Gal4 construct was co-transfected into 293T cells with either the KLF5-Luc construct or empty vector followed by simulated moderate or severe I/RI for 24 h. The transfection efficiency was corrected by the β-galactosidase controls. Data are shown as the mean of four separate experiments ± SEM. **P < 0.01 versus cells with simulated moderate I/RI (Dunnett’s test). d Expression of KLF5 protein determined by immunofluorescence in 293T cells transfected with HIF-1α-WT or HIF-1α-N803A-mutant for 48 h (n = 4). Scale bars, 100 μm. e The protein expression of α-SMA and collagen-1 in 293T cells transfected with HIF-1α-WT or HIF-1α-N803A-mutant for 48 h was determined by Western blotting. Data were obtained from four independent experiments. **P < 0.01, by Bonferroni post hoc test after 2-way ANOVA.