#4478 HIF-1α REGULATED LNCRNA-ATP6V0E2-AS1 MEDIATES HYPOXIA-INDUCED MITOPHAGY IN RENAL TUBULAR CELLS

Abstract Background and Aims Mitophagy activation is crucial for hypoxia signaling in acute kidney injury (AKI). Selective removal of damaged mitochondria mediated through a concerted function coding non-coding RNA expressions. Insights on HIF-1α lncRNA-regulated mitophagy mechanism are not known. The study aims to investigate the role hypoxia-inducible factor 1α (HIF-1α) regulated long (lncRNA) ATP6V0E2-AS1 (AKI) by examining its effect mitophagy. Method proteins (PINK1, p-PARKIN, LC3) were determined western blot analysis. Immunofluorescence studies PINK1 mitochondrial translocation LC3/TOMM20 localization using confocal interaction with lncRNA-ATP6V0E2-AS1 promoter binding activity was evaluated chromatin immunoprecipitation between analyzed dual-luciferase reporter assay. Results Hypoxia upregulated PINK1, LC3 expressions, mitophagosome HK-2 cells. Overexpression knockdown hypoxia-regulated significantly PINK1/p-PARKIN subsequent co-localization, formation. shHIF-1α cells reveals that mediates regulation under hypoxic conditions. In detail, binds down-regulates expression hypoxia. Deficiency both reverted suppression Further, post-transcriptionally regulates RNA-RNA interaction. Conclusion Altogether, our shows novel findings hypoxia-induced renal tubular Thus, downregulated critical HIF-1α/ATP6V0E2-AS1/PINK1 axis.