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Abstract
Purpose The current study aims to examine the effects of advanced glycation end products (AGEs) on the microRNA (miRNA) expression profile in the kidney tissues of rats. Methods Wistar rats were randomly divided into three equal experiment groups: the AGE group, the RSA group, and the control group. The rats in the AGE group and the RSA group were administered with advanced glycation end products (AGEs) and rat serum albumin (RSA) via the tail vein, respectively, whereas the control group received PBS. Total RNA was prepared from the rat kidney tissues, and the miRNA expression profiles in different experiment groups were compared by microarray analysis. The expression levels of selected differential miRNAs were verified by RT-qPCR. Target gene prediction was conducted using algorithms such as TargetScan, miRanda, and PICTar. Functional analysis was performed to determine the putative biological roles of the validated miRNAs. Results The microarray study revealed 451 upregulated and 320 downregulated miRNAs in the AGE group compared with the RSA group (p < 0.05). Seven miRNAs, including miR-21-5p, miR-92b-3p, miR-140-3p, miR-196a-5p, miR-181b-5p, miR-186-5p, and miR-192-5p, were screened and verified using RT-qPCR, of which, the change of miR-92b-3p was the most obvious according to the miRNA expression different multiple and p < 0.05). Seven miRNAs, including miR-21-5p, miR-92b-3p, miR-140-3p, miR-196a-5p, miR-181b-5p, miR-186-5p, and miR-192-5p, were screened and verified using RT-qPCR, of which, the change of miR-92b-3p was the most obvious according to the miRNA expression different multiple and Conclusion The results of the current study suggested that miR-92b-3p could mediate AGE-induced development of renal abnormalities through targeting Smad7 in rats with DN.
Highlights
Diabetic nephropathy (DN) is a leading cause of death among diabetic patients and a major contributing factor to end-stage renal diseases [1]
Based on the above findings, the current study aims to probe whether advanced glycation end products (AGEs) could affect the miRNA expression profile in rat kidneys
H&E staining found the kidneys harvested from the AGE group to exhibit clear visual signs of mesangial cell hyperplasia and extracellular matrix (ECM) expansion (Figure 1(a))
Summary
Diabetic nephropathy (DN) is a leading cause of death among diabetic patients and a major contributing factor to end-stage renal diseases [1]. Common pathological features of DN include the aggregation of extracellular matrix (ECM) proteins, the proliferation and hypertrophy of mesangial cells (MMCs), as well as the dysfunction of glomerular podocytes [2]. Patients with advanced DN can develop glomerular lesions and proteinuria. The pathogenesis and treatment of DN have become a main focus of clinical research on diabetes and renal diseases. It is generally accepted that mutual reinforcement of metabolic dysregulation and hemodynamic abnormalities contributes to a vicious cycle of deteriorating renal pathologies in patients with chronic hyperglycemia [4, 5]. The exact mechanism for DN pathogenesis is extremely complex and remains poorly understood, which has hampered the development of effective diagnostic tools and therapies
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