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Long noncoding RNA NEAT1 accelerates the proliferation and fibrosis in diabetic nephropathy through activating Akt/mTOR signaling pathway

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机构: [1]Shanghai Jiao Tong Univ, Shanghai Tongren Hosp, Sch Med, Endocrinol Dept, Shanghai, Peoples R China [2]Xuzhou Med Univ, Huaian Peoples Hosp 2, Dept Nephrol, Huaian, Peoples R China [3]Xuzhou Med Univ, Affiliated Huaian Hosp, Huaian, Peoples R China
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关键词: Akt mTOR signaling diabetic nephropathy NEAT1

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Accumulating evidence has indicated the significant roles of long noncoding RNAs (lncRNAs) in the pathophysiology of diabetic nephropathy (DN). LncRNA nuclear enriched abundant transcript 1 (NEAT1) has been reported to exert a key role in the progression of several diseases including diabetes. However, the role of NEAT1 in the regulation of DP progression remains barely known. Therefore, our study aimed to investigate the role of NEAT1 in a streptozotocin-induced diabetes model (DM) of rats and glucose-induced mouse mesangial cell models. Currently, we found that NEAT1 was greatly upregulated in DM rats and glucose-induced mice mesangial cells, in which a high activation of Akt/mTOR signaling was also observed. Then, it was shown that knockdown of NETA1 was able to reduce renal injury in DM rats obviously. In addition, cell counting kit-8 assay and 5-ethynyl-2-deoxyuridine assay were carried out and we observed downregulation of NEAT1 significantly inhibited mesangial cell proliferation. Meanwhile, extracellular matrix proteins and messenger RNA (transforming growth factor 1, fibronectin, and collagen IV) expression was dramatically restrained by silencing of NEAT1 in the high glucose-induced mesangial cells. Finally, knockdown of NEAT1 greatly reduced the expression of the phosphorylation of Akt and mammalian target of rapamycin (mTOR) in vitro. These findings revealed that the decrease of NEAT1 repressed the proliferation and fibrosis in DN via activating the Akt/mTOR signaling pathway, which might represent a novel pathological mechanism of DN progression.

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出版当年[2018]版:
大类 | 2 区 生物
小类 | 2 区 生理学 3 区 细胞生物学
最新[2025]版:
大类 | 3 区 生物学
小类 | 3 区 细胞生物学 3 区 生理学
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出版当年[2017]版:
Q1 PHYSIOLOGY Q2 CELL BIOLOGY
最新[2023]版:
Q1 PHYSIOLOGY Q2 CELL BIOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2017版] 出版当年五年平均 出版前一年[2016版] 出版后一年[2018版]

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第一作者机构: [1]Shanghai Jiao Tong Univ, Shanghai Tongren Hosp, Sch Med, Endocrinol Dept, Shanghai, Peoples R China [*1]Endocrinology Department, School of Medicine, Shanghai Tongren Hospital, Affiliated to Shanghai Jiao Tong University, Shanghai, China
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通讯机构: [1]Shanghai Jiao Tong Univ, Shanghai Tongren Hosp, Sch Med, Endocrinol Dept, Shanghai, Peoples R China [*1]Endocrinology Department, School of Medicine, Shanghai Tongren Hospital, Affiliated to Shanghai Jiao Tong University, Shanghai, China
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