A novel long non-coding RNA CYP4B1-PS1-001 regulates proliferation and fibrosis in diabetic nephropathy

被引:106
作者
Wang, Min [1 ]
Wang, Suyu [1 ]
Yao, Di [1 ]
Yan, Qin [2 ]
Lu, Weiping [1 ]
机构
[1] Nanjing Med Univ, Huaian Peoples Hosp 1, Dept Endocrinol & Metab, 6 Beijing Rd West, Huaian 223300, Jiangsu, Peoples R China
[2] Nanjing Med Univ, Dept Microbiol, Nanjing 210029, Jiangsu, Peoples R China
关键词
Diabetic nephropathy; IncRNA; Proliferation; Fibrosis; MOLECULAR-MECHANISMS; CELL-PROLIFERATION; GENE; CANCER; INHIBITION; PREVALENCE; EXPRESSION; DISEASE;
D O I
10.1016/j.mce.2016.02.020
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Diabetic nephropathy is an important microvascular complication of diabetes, and the incidence of end stage renal disease caused by it are rising annually. Long non-coding RNAs (IncRNAs) are widely regarded to associate with the occurrence and development of various diseases; however, the relationship between IncRNAs and diabetic nephropathy remains largely unknown. This work studied the effect of IncRNAs on diabetic nephropathy pathogenesis. LncRNA microarrays were initially used to detect IncRNAs with altered expression in three cases of kidney tissue from db/db mice with diabetic nephropathy. LncRNAs with differential expression (>2-fold) could be considered candidates. Particularly, CYP4B1-PS1-001 was significantly downregulated in response to early diabetic nephropathy in vitro and in vivo, while overexpression of CYP4B1-PS1-001 inhibited proliferation and fibrosis of mesangial cells. Overall, our data indicate the potential role of CYP4B1-PS1-001 in the proliferation and fibrosis of mice mesangial cells as the prominent features during early stage of diabetic nephropathy, which extend the relationship between IncRNAs and diabetic nephropathy, and may provide a potential therapeutic target and molecular biomarker for the disease. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:136 / 145
页数:10
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