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. 2012 Jan 24;122(2):693–710. doi: 10.1172/JCI60214

Figure 3. Influence of renal ischemia on ENT expression.

Figure 3

(A) Ent1 and Ent2 transcript levels in kidneys exposed to sham operation (Sham) or 30 minutes of ischemia, followed by reperfusion for the indicated time periods assessed by real-time RT-PCR relative to β-actin (n = 4 independent experiments). (B) Ent1 and Ent2 protein levels assessed by Western blotting (β-actin to control for loading conditions; 1 representative blot of 3 is shown). (C) Comparison of immunoreactivity for Ent1 and Ent2 in kidneys exposed to 30 minutes of renal ischemia and 2 hours of reperfusion or sham-operated controls (original magnification, ×400; fluorescent green: counterstaining for proximal tubules; fluorescent red [arrows]: staining for Ent1 or Ent2; 1 representative image of 3 is displayed). (D) Relative expression levels of Ent1 or Ent2 transcript in isolated tubules or glomeruli, relative to β-actin by real-time RT-PCR (n = 4 independent experiments). (E) ENT1 and ENT2 transcript levels in cultured HK-2 cells exposed for the indicated time periods to ambient hypoxia (1% oxygen) assessed by real-time RT-PCR relative to β-actin (n = 4 independent experiments). (F) ENT1 and ENT2 protein levels from HK-2 cells exposed to indicated time periods to ambient hypoxia (1% oxygen) and assessed by Western blot (β-actin to control for loading conditions; 1 representative blot of 3 is shown).