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LINC00162 participates in the pathogenesis of diabetic nephropathy via modulating the miR-383/HDAC9 signalling pathway

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机构: [1]Kunming Med Univ, Dept Nephrol, Affiliated Hosp 1, Kunming, Yunnan, Peoples R China [2]Kunming Med Univ, Yunnan Key Lab Lab Med, Affiliated Hosp 1, Kunming, Yunnan, Peoples R China [3]Kunming Med Univ, Kunming, Yunnan, Peoples R China [4]Nanjing Univ, Jinling Hosp, Dept Nutr, Sch Med, Nanjing, Jiangsu, Peoples R China [5]Kunming Med Univ, Inst Gastroenterol, Dept Gastrointestinal Surg, Affiliated Hosp 1, 295 Xichang Rd, Kunming 650032, Yunnan, Peoples R China [6]Sichuan Univ, West China Hosp, Dept Nephrol, 37 Guoxue Alley, Chengdu 610041, Sichuan, Peoples R China [7]Department of Gastrointestinal Surgery, Institute of Gastroenterology, The First Affiliated Hospital of Kunming Medical University, No.295, Xichang Road, Kunming 650032, Yunnan, China [8]Department of Nephrology, West China Hospital, Sichuan University, No. 37, Guoxue Alley, Chengdu 610041, Sichuan, China
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关键词: Diabetic nephropathy podocyte apoptosis LINC00162 miR-383 HDAC9

摘要:
Diabetic nephropathy (DN) is a common chronic complication of diabetes. In this study, we aimed to explore the potential role of lncRNA LINC-00162 in the pathogenic process of DN. LncRNA microarray analysis, real-time PCR, IHC computational analysis and luciferase assay were performed to explore the regulatory relationship among LINC00162, miR-383 and HDAC9. There was an obvious difference between T2D + DN and T2D - DN patients in their levels of eGRF and albuminuria. A significant difference was observed between T2D + DN and T2D - DN groups in terms of their LINC00162 expression. In particular, LINC00162 and HDAC9 were highly expressed, while miR-383 was lowly expressed in tissues derived from the T2D + DN group compared with those in tissues derived from the T2D - DN group. MiR-383 was able to bind to LINC00162, while HDAC9 was a direct downstream target of miR-383 with a complementary miR-383 binding site located in the 3 ' UTR of HDAC9. LINC00162 reduced miR-383 expression and further up-regulated HDAC9 expression, while miR-383 mimics reduced HDAC9 expression under a dose-dependent manner. In summary, we suggested for the first time that down-regulation of LINC00162 was associated with the development of DN in T2D via the up-regulation of miR-383 expression and reduction of HDAC9 expression.

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出版当年[2021]版:
大类 | 2 区 医学
小类 | 2 区 生物工程与应用微生物 2 区 工程:生物医学 3 区 材料科学:生物材料
最新[2023]版:
大类 | 3 区 生物学
小类 | 3 区 生物工程与应用微生物 3 区 工程:生物医学 4 区 材料科学:生物材料
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出版当年[2020]版:
Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Q1 ENGINEERING, BIOMEDICAL Q2 MATERIALS SCIENCE, BIOMATERIALS
最新[2023]版:
Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Q2 ENGINEERING, BIOMEDICAL Q2 MATERIALS SCIENCE, BIOMATERIALS

影响因子: 最新[2023版] 最新五年平均 出版当年[2020版] 出版当年五年平均 出版前一年[2019版] 出版后一年[2021版]

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第一作者机构: [1]Kunming Med Univ, Dept Nephrol, Affiliated Hosp 1, Kunming, Yunnan, Peoples R China [2]Kunming Med Univ, Yunnan Key Lab Lab Med, Affiliated Hosp 1, Kunming, Yunnan, Peoples R China
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通讯机构: [7]Department of Gastrointestinal Surgery, Institute of Gastroenterology, The First Affiliated Hospital of Kunming Medical University, No.295, Xichang Road, Kunming 650032, Yunnan, China [8]Department of Nephrology, West China Hospital, Sichuan University, No. 37, Guoxue Alley, Chengdu 610041, Sichuan, China
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