The pathogenesis of acute kidney injury (AKI) is not fully understood. To date, the exact role and regulatory mechanism of long non-coding RNA (lncRNA)136131 in AKI remains unclear. Here, we demonstrate that lncRNA136131 in BUMPT cells is induced by antimycin A. Furthermore, after incubating BUMPT cells in antimycin for two hours, lncRNA136131 prevented BUMPT cell apoptosis and cleaved caspase-3 expression. Mechanistically, lncRNA136131 sponged miR-378a-3p and then increased the expression of Rab10 to suppress apoptosis. Finally, I/R-induced decline of renal function, tubular damage, renal tubular cells apoptosis, and the upregulation of cleaved caspase-3 were aggravated by lncRNA136131 siRNA. In contrast, this effect was attenuated by the overexpression of lncRNA136131. In conclusion, lncRNA136131 protected against I/R-induced AKI progression by targeting miR-378a-3p/Rab10 and may be utilized as a novel target for AKI therapeutics.
Keywords: AKI; Rab10; apoptosis; lncRNA; miR-378a-3p.