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. 2017 Oct 11;314(2):F293–F305. doi: 10.1152/ajprenal.00364.2017

Fig. 9.

Fig. 9.

P2X7 receptor activation exacerbates renal tubular necrosis after renal IR (RIR) injury in PAD4 wild-type (WT) mice but not in PAD4-deficient (KO) mice. PAD4 WT and PAD4 KO mice were pretreated with vehicle or with 5 mg/kg BzATP ip 24 h before being subjected to 20 min RIR injury. A: representative H&E images (N = 4) of PAD4 mice subjected to 20 min renal ischemia and 24 h of reperfusion (magnification 200×) after vehicle or BzATP treatment. B: the renal injury score (scale: 0–4, N = 4) for histology grading was used to grade renal tubular necrosis 24 h after 20 min renal IR. Renal tubular necrosis was worse in PAD4 WT mice treated with BzATP before 20 min RIR compared with WT mice treated with vehicle before 20 min RIR. As demonstrated previously, PAD4 deficiency resulted in significant reduction in renal tubular injury score after RIR compared with PAD4 WT mice. Moreover, BzATP failed to exacerbate renal tubular necrosis in PAD4 KO mice subjected to 20 min RIR. *P < 0.05 vs. vehicle-treated PAD4 wild-type mice subjected to RIR. Error bars represent 1 SE.