The proliferation of mesangial cells (MCs) is a characteristic feature of glomerular diseases, including lupus nephritis, IgA nephropathy, membranoproliferative glomerulonephritis and diabetic nephropathy (1). Furthermore, in animal models of nephritis, MC proliferation often occurs before mesangial

Hyperproliferation of mesangial cells (MCs) is the central pathological feature observed in certain human renal diseases. Furthermore, the long non‐coding RNA uc.412 is regulated by transforming growth factor β1 in mesangial cells in vitro. The present study aimed to investigate whether uc.412 serves a role in renal fibrosis and whether it may be consid‐ ered as a therapeutic target in mesangial proliferative kidney diseases. The results demonstrated that uc.412 overexpression significantly increased MC proliferation. The transcriptional profile of MCs overexpressing uc.412 was assessed by RNA sequencing. A total of 462 up‐ and 843 downregulated genes were identified (|fold change| ≥1.5), and reverse transcrip‐ tion‐quantitative PCR was used to determine the expression of these differentially expressed genes (DEGs). Subsequently, the potential function of these DEGs was determined by bioinformatics analyses. The results indicated that these DEGs were involved in numerous signaling pathways associated with MC proliferation. The downstream association between up‐ and downregulated genes was constructed via the STRING database. The protein‐protein interaction network indicated that serpin family E member 1 and matrix metallopeptidase 3 may be hub proteins. In conclusion, the present study provided novel insight into the role of uc.412 in MC proliferation, which may aid in the development of novel treatment for mesangial proliferative kidney diseases. Introduction The proliferation of mesangial cells (MCs) is a characteristic feature of glomerular diseases, including lupus nephritis, IgA nephropathy, membranoproliferative glomerulonephritis and diabetic nephropathy (1). Furthermore, in animal models of nephritis, MC proliferation often occurs before mesangial sclerosis and the glomerulosclerosis, and is associated with the increase in extracellular matrix synthesis (2). Regulation of MC proliferation may therefore represent a potential treat‐ ment option for numerous kidney diseases (3). Transforming growth factor (TGF)‐β1 is a cytokine that promotes fibrosis in chronic renal diseases, and may trigger and regulate various types of pathophysiological process. For example, TGF‐β contributes to glomerular extracellular matrix accumulation by stimulating MCs to produce type I, III and IV collagen, laminin, fibronectin and heparan sulphate proteoglycans, as well as by inhibiting matrix degradation, which contributes to the development of glomerulosclerosis (4). However, TGF‐β1 also has anti‐inflammatory properties in certain pathological conditions. For example, TGF‐β blockade increased kidney inflammation, which was characterized by the upregulation of MCP1, proinflammatory chemokines and the infiltration of monocytes/macrophages in the kidneys (5). Considering these situations, TGF‐β1 may not be an optimal therapeutic target for kidney disease (5). It is therefore crucial to explore the TGF‐β1‐associated mechanisms in order to identify its therapeutic targets. Long non‐coding (lnc) RNAs are defined as transcripts of >200 nucleotides in length that are not translated into proteins (6). Compared with protein‐coding genes, lncRNAs are more conserved and specific to organs, tissues, cell types, developmental stages and disease conditions. In addition, lncRNAs are considered as better therapeutic targets in kidney diseases compared with protein‐coding transcriptomes (7). It has been reported that lncRNAs may be more responsible for the early development of diabetic nephropathy compared with protein‐coding genes (8). For example, the lncRNA LINC01619 contributes to the development of diabetic nephropathy, as it can regulate microRNA (miR)‐27a/forkhead box protein O1 and endoplasmic reticulum stress, resulting Gene expression profiling analysis reveals that the long non‐coding RNA uc.412 is involved in mesangial cell proliferation MINYI YU1,2*, ZHENG GUAN1,3*, SHANWEN LI1*, XIANLI WEN1, HUIMIN SHI1, GAOTING QU1, XIAOYU LU1, XIANYI ZHU1, BIN WANG4, QIHUA FENG2, WEIHUA GAN1 and AIQING ZHANG1 1Department of Pediatric Nephrology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210003; 2Department of Rheumatology, Children's Hospital of Soochow University, Suzhou, Jiangsu 215000; 3Department of Pediatrics, Yangzhou Maternal and Child Care Service Center, Yangzhou, Jiangsu 225000; 4Institute of Nephrology, Zhong Da Hospital, Southeast University, Nanjing, Jiangsu 210000, P.R. China Received March 24, 2019; Accepted August 8, 2019 DOI: 10.3892/mmr.2019. 10753 Correspondence to: Professor Aiqing Zhang, Department of Pediatric Nephrology, The Second Affiliated Hospital of Nanjing Medical University, 262 Zhongshan North Road, Nanjing, Jiangsu 210003, P.R. China E‐mail: njaiqing@njmu.edu. cn *Contributed equally