Effect of lncRNA-MIAT on kidney injury in sepsis rats via regulating miR-29a expression

Y. Zhang, Y.-Y. Zhang, F. Xia, A.-X. Yang, J.-X. Qian, H. Zhao, W.-Y. Tao

Department of Critical Care Medicine, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou, China. 815381426@qq.com

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• Nephrology

OBJECTIVE: The long non-coding ribonucleic acid (lncRNA)-myocardial infarction associated transcript (MIAT) has been demonstrated to serve as a key regulator in various physiological and pathological processes. This study aims to explore whether lncRNA-MIAT regulates the expression of micro RNA (miR)-29a to affect kidney’s injury in sepsis rats.

MATERIALS AND METHODS: A total of 30 healthy male Sprague-Dawley (SD) rats were randomly divided into experimental group and control group. Rats in the experimental group were injected with lipopolysaccharide (LPS) through the tail vein to prepare the model of sepsis-induced kidney injury, while those in the control group with the equal volume of normal saline. After the levels of serum creatinine (SCr) and blood urea nitrogen (BUN) in rats were determined to ascertain successful modeling, fluorescence quantitative Real-time polymerase chain reaction (qRT-PCR) was performed to measure the expression levels of the lncRNA-MIAT and miR-29a messenger RNAs (mRNAs) in renal tissues. The normal rat kidney epithelial (NRK-52E) cell line was cultured in vitro, and the model was established in vitro via LPS to study the influences of lncRNA-MIAT and miR-29a on the kidney injury in sepsis rats. Moreover, cell apoptosis was detected using Western blotting.

RESULTS: According to the results of the rat in vivo experiment and NRK-52E cell line in vitro experiment, the model of kidney injury was established successfully, and compared with the control group, experiment group had significantly raised SCr and BUN levels (p<0.01) and a remarkably increased lincRNA-MIAT gene expression level (p<0.01), but a substantially decreased miR-29a gene expression level (p<0.01). Additionally, when the expression of lncRNA-MIAT was up-regulated, the expression of miR-29a was prominently decreased (p<0.01), but that of the cell apoptosis gene cysteine-aspartic proteases (Caspase)-8 protein was remarkably increased (p<0.01). However, the expression of Caspase-8 protein was significantly lowered (p<0.01) once the expression of miR-29a was up-regulated.

CONCLUSIONS: LncRNA-MIAT may bind to miR-29a to participate in sepsis-related kidney injury.

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