Fig. 1: HIF-1α CTAD KO results in severe renal injury in I/R-induced AKI. | Cell Death & Disease

Fig. 1: HIF-1α CTAD KO results in severe renal injury in I/R-induced AKI.

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

Fig. 1

a Construction strategy for HIF-1α CTAD−/− mouse. b Schematic representation of the proposed HIF-1α CTAD KO. c SCr and BUN levels on day 1 following 35 min of ischemia/reperfusion-induced renal injury (I/RI) (n = 6). d Quantitative real-time polymerase chain reaction (qRT-PCR) analysis of KIM-1 expression. The relative levels were normalized to β-actin (n = 6). e Representative images of KIM-1 staining (n = 6). Scale bars, 50 µm. f Representative histological changes (periodic acid-Schiff [PAS] staining) on day 1 following 35 min of I/RI (left, n = 6). Scale bar, 100 µm. The quantification of tubular injury based on PAS staining (right, n = 6). g mRNA expression of inflammatory factors (monocyte chemoattractant protein-1 [MCP-1], tumor necrosis factor-α [TNF-α], and interleukin-1β [IL-1β]) in the I/R injured kidney assessed by qRT-PCR. The relative levels were normalized to β-actin (n = 6). h. Representative F4/80 stained kidney sections from I/R injured mice (left). Scale bars, 50 µm. The semiquantitative population of F4/80+ macrophages infiltrating the I/R injured kidney (right). Data are shown as mean ± SEM of 6 mice. **p-value < 0.01 versus the WT mice (t-test).

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