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Abstract: PO0186

Exploration of the Mitochondria Genes Alteration in AKI

Session Information

Category: Acute Kidney Injury

  • 101 AKI: Epidemiology, Risk Factors, and Prevention

Authors

  • Li, Shensen, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu, China
  • Liu, Qingqing, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu, China
  • Shen, Haiyan, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu, China
  • Deng, Bingquan, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu, China
  • Li, Wenwen, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu, China
  • Cao, Changchun, Sir Run Run Hospital Nanjing Medical University, Nanjing, Jiangsu, China
Background

Acute kidney injury (AKI) is one of the most common complications in clinic, especially in critical ill patients. Recently, the fundamental function of mitochondria in acute kidney injury and repair have gradually been noticed while the mechanism still unclear. Therefore, we aimed to identify the change pattern of mitochondria alteration associated gene in AKI through Gene Expression Omnibus (GEO) database analysis and AKI animal model verification.

Methods

A total of 1893 genes involved in mitochondria function and metabolism were screened from Gene Ontology (GO) database and defined as GO terms in mitochondria metabolism. Meanwhile, 2 studies invested transcriptome differences in renal ischemia reperfusion injury (GSE98622 and GSE99703) were extracted from GEO database. By crossing GO terms and 2 datasets from GEO database, 69 and 62 mitochondria metabolism genes were identified in GSE98622 and GSE99703 separately. Among which, 23 genes were overlapped in 2 datasets and verified by real-time PCR in 2 kinds of AKI model (ischemic renal reperfusion injury model and cisplatin induced AKI model).

Results

Through GO and KEGG enrichment analysis, these differentially expressed genes (DEGs) were allocated to peroxisome, butanoate metabolism, arginine and proline metabolism, neurotrophin signaling pathway and metabolic pathways. Protein-protein interaction analysis demonstrated that Hao2, Acsm3, Amacr, Aadat may play vital roles of mitochondrial regulation in AKI. The results of real-time PCR shown that 3 genes were significantly increased in both two kinds of AKI model (Arg2, Clu, Lgals3) and 12 genes were decreased (Aadat, Acsm3, Agps, Ak4, Amacr, Bdh1, Gatm, Hao2, Isoc2b, Mpv17l, Nat8f1, Nudt19), while others were not altered in animal model or had no consistency changes between 2 kinds of AKI model.

Conclusion

We have identified 23 DEGs were associated with mitochondria metabolism in I/R AKI by using bioinformatic technology. Among these genes, GO and KEGG analysis suggests that the DEGs are mainly enriched in lipid metabolism, amino acid metabolism pathway and tightly associated with peroxisome. Furthermore, 15 DEGs were revalidated in kidney of two kinds of AKI mouse model (I/R AKI and Cisplatin-AKI).

Funding

  • Government Support – Non-U.S.