KEYWORDS miR-10a, PIK3CA, PI3K/AKT signaling pathway, renal ischemia reperfusion 2 Abstract Background To investigate the effect of miR-10a on PI3K/AKT signaling pathway. The ischemia-reperfusion injury models of rats were simulated in vivo . Methods RT-PCR was used to test the expression of miR-10a. The serum creatinine and urea nitrogen levels were determined. The pathological changes and the apoptosis of renal cells were observed. The model of HK-2 cells with hypoxia-reoxygenation was

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... shed in vitro. The cell proliferation and apoptosis rate were tested by CCK8, clone formation and flow cytometry, respectively. The apoptosisrelated proteins and PIK3CA and PI3K/AKT signaling pathway-related proteins were detected by Western blot both in vivo and intro . The dual luciferase assay was used to verify whether PIK3CA is a target gene of miR-10a. PIK3CA gene was over-expression or silenced. The transfection efficiency was verified by RT-PCR and the above experiments were repeated. Results Compared with I/R group, miR-10a RNA was significantly increased in renal tissue of miR-10a group, serum Cr and BUN levels, and renal injury score and apoptosis index were significantly increased, while the expression of PI3K/AKT signaling pathway-related proteins were significantly inhibited. However, the indicators above were contrary in anti-miR group. In comparison with H/R group, miR-10a RNA expression was remarkably increased in miR-10a cells and the cell proliferation was inhibited. The apoptosis rate was increased and the expression of PI3K/AKT signaling pathway-related proteins were down-regulated. However, the indicators above were contrary in anti-miR group. Conclusion miR-10a can aggravate the ischemia-reperfusion-induced renal injury in rats by targeting PIK3CA and inhibitingPI3K/AKT signaling pathway. Background Kidney transplantation is often accompanied with unavoidable acute renal failure, the main cause of which is considered to renal ischemia-reperfusion injury (IRI), in addition, it is also considered to be an