The expression profiles of
miRNAs in serum from patients with
sepsis-induced AKI (n = 6),
sepsis-non AKI (n = 6), and healthy volunteers (n = 3) were investigated by microarray assay and validated by quantitative PCR (qPCR). The targets of the differentially expressed
miRNAs were predicted by Target Scan, mirbase and Miranda. Then the significant functions and involvement in signaling pathways of gene ontology (GO) and KEGG pathways were analyzed. Furthermore, eight
miRNAs were randomly selected out of the differentially expressed
miRNAs for further testing by qPCR.
RESULTS: qPCR analysis confirmed that the expressions levels of hsa-miR-23a-3p,
hsa-miR-4456, hsa-miR-142-5p, hsa-miR-22-3p and hsa-miR-191-5p were significantly lower in patients with
sepsis compared with the healthy volunteers, while hsa-miR-4270, hsa-miR-4321, hsa-miR-3165 were higher in the
sepsis patients. Statistically, miR-4321; miR-4270 were significantly upregulated in the
sepsis-induced AKI compared with
sepsis-non AKI, while only miR-4321 significantly overexpressed in the
sepsis groups compared with control groups. GO analysis showed that biological processes regulated by the predicted target genes included diverse terms. They were related to kidney development, regulation of
nitrogen compound metabolic process, regulation of cellular metabolic process, cellular response to oxidative stress, mitochondrial outer membrane permeabilization, etc. Pathway analysis showed that several significant pathways of the predicted target genes related to oxidative stress. miR-4321 was involved in regulating AKT1, mTOR and NOX5 expression while miR-4270 was involved in regulating PPARGC1A, AKT3, NOX5, PIK3C3, WNT1 expression. Function and pathway analysis highlighted the possible involvement of
miRNA-deregulated mRNAs in oxidative stress and
mitochondrial dysfunction.
CONCLUSION: This study might help to improve understanding of the relationship between serum
miRNAs and
sepsis-induced AKI, and laid an important foundation for further identification of the potential mechanisms of
sepsis-induced AKI and oxidative stress and
mitochondrial dysfunction.