Fig. 4: HK2 transcriptionally regulated by the HIF-1α C-TAD protects against hypoxia-induced tubule injury. | Cell Death & Disease

Fig. 4: HK2 transcriptionally regulated by the HIF-1α C-TAD protects against hypoxia-induced tubule injury.

From: Activation of HIF-1α C-terminal transactivation ___domain protects against hypoxia-induced kidney injury through hexokinase 2-mediated mitophagy

Fig. 4

a, c qRT-PCR analysis of HK2 and KIM-1 expression in the tubular cells with H/R. The relative level was normalized to β-actin (n = 4). b Western blotting analysis of HK2 expression in the tubular cells with H/R (n = 4). d, f HK2 and KIM-1 mRNA expression were analyzed in primary TECs with H/R before HIF-1α CTAD was overexpressed with adenovirus (Ad-CTAD). The relative level was normalized to β-actin (n = 4). e Western blotting analysis of HK2 expression in the primary TECs with H/R before HIF-1α CTAD was overexpressed with adenovirus (Ad-CTAD) (n = 4). g mRNA expression of inflammatory factors (MCP-1, TNF-α, and IL-1β) in the primary TECs with H/R after HIF-1α CTAD was overexpressed with adenovirus (Ad-CTAD). The relative levels were normalized to β-actin (n = 4). h Luciferase assay results corrected for transfection efficiency using β-galactosidase are shown as an average of 4 separate experiments ± SEM. i ChIP assay shows binding of HIF-1 to the HK2 promoter (n = 4). j KIM-1 mRNA expression was analyzed in primary TECs with H/R after HK2 was overexpressed with adenovirus (Ad-HK2). The relative level was normalized to β-actin (n = 4). k mRNA expression of inflammatory factors (MCP-1, TNF-α, and IL-1β) in the primary TECs with H/R after HK2 was overexpressed with adenovirus (Ad-HK2). The relative levels were normalized to β-actin (n = 4). **p-value < 0.01 versus the NC group (t-test or Mann–Whitney U test).

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