[No authors listed]
Acute kidney injury is mostly reversible, and hepatocyte growth factor (HGF) has a relevant role in the tissue repair. MicroRNA (miR)-26a is an endogenous modulator of HGF. The role of miR-26a in the kidney repair process was evaluated in Wistar rats submitted to an acute kidney injury model of rhabdomyolysis induced by glycerol (6âmL/kg). Animals were evaluated 3, 12, 48, 96, and 120âhours after glycerol injection. Serum creatinine (SCr) and gene expression of HGF, c-met, signal transducer and activator of transcription 3 and miR-26a were estimated. Also, tubular NK52E cells were transfected with anti-miR26a and stimulated with Fe3+ for 24âhours to mimic the effects of myoglobin in vitro. SCr was highest after 48âhours. After 96âhours, SCr started to decrease, characterizing the recovery phase, with normalization after 120âhours. HGF expression increased during the onset phase (3âhours), with a low relationship with miR-26a. In contrast, in the recovery phase, the increase in miR-26a was coincident with HGF messenger RNA suppression, suggesting that in the recovery phase, miR-26a may have a role in HGF modulation. Fe3+ induced cellular death after 3âhours and proliferation after 24âhours. There was no correlation between miR-26a and during the death phase; however, during the proliferation phase, an increase in duanyu18133 was paralleled with a decrease in miR-26a. miR-26a silencing induced increases in cell viability and the phosphorylated form of duanyu18133 protein expression in cells receiving Fe3+ . In conclusion, miR-26a may have a key role in modulating HGF levels after its proliferative effects have been triggered.
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