Original Article


MicroRNA expression profile by next-generation sequencing in a novel rat model of contrast-induced acute kidney injury

Yong Liu, Bowen Liu, Yuanhui Liu, Shiqun Chen, Junqing Yang, Jin Liu, Guoli Sun, Wei-Jie Bei, Kun Wang, Zhujun Chen, Ning Tan, Jiyan Chen

Abstract

Background: MicroRNAs (miRNAs) are known to regulate most biological processes including contrast-induced acute kidney injury (CI-AKI). Few studies have investigated microRNA (miRNAs) expressions in a novel rat model of CI-AKI using nonionic low-osmolar iodic contrast medium Ultravist, and performed gene ontology (GO) categories analysis.
Methods: In this study, kidney tissues were collected from Sprague-Dawley rats at 24 h after contrast-exposure (CI-AKI) and saline-administration (control). MiRNAs microarray assays were used to detect miRNAs in the kidney tissue by next-generation sequencing. Real-time PCR was performed to verify the microarray assays results. All significant differently expressed miRNAs were analyzed by GO categories and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways.
Results: Of the 173 detected miRNAs, 22 were down-regulated (miR-328a-5p, miR-31a-5p, miR-377-3p, et al.) and 19 were up-regulated (miR-3558-5p, miR-34c-3p, miR-384-5p, et al.) in the kidneys of CI-AKI rats according to log2 (fold change, control) >1, P<0.001 as significant differently expressed miRNAs, which included new differently expressed miRNAs, such as miRNA-1949 and miR-3558. The results showed that a large set of genes involved in essential biological processes were targeted by these miRNAs, such as dysfunction metabolic process, apoptotic process, and endoplasmic reticulum stress, in addition to genes implicated in signaling pathways involved in inflammation and dysfunctional metabolism, including AGE-RAGE signaling pathway and glycerophospholipid metabolism.
Conclusions: The 41 miRNAs identified were differentially expressed in the kidneys of a novel rat model of CI-AKI, and thus possess the potential to serve as novel biological markers and new molecular targets for CI-AKI.

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