Knockdown of miR-21 exacerbates IR injury in mice kidneys following delayed IPC and IR by upregulation of PDCD4 expression, and exacerbates damage of microvascular endothelial cells. (A) PDCD4 protein expression was decreased in mice kidneys exposed to delayed IPC and IR. (B) miR-21 knockdown resulted in upregulation of PDCD4 protein expression. (C) Delayed IPC significantly attenuated apoptosis of vascular endothelial cells as indirectly determined by microvascular permeability 24 h after IR, whereas locked nucleic acid-modified anti-miR-21 oligonucleotide treatment exacerbated Evans blue dye leakage from renal vascular cells. Data are presented as the mean ± standard error of the mean. n=5–6 per group; *P<0.05 and **P<0.01 vs. Sham + IR group; #P<0.05 vs. scrambled control group. IPC, ischemic preconditioning; IR, ischemia/reperfusion; miR-21, microRNA-21; PDCD4, programmed cell death protein 4.