炎症
糖尿病肾病
纤维化
CCL19型
活力测定
小RNA
生物
癌症研究
趋化因子
医学
细胞
免疫学
病理
肾
趋化因子受体
内分泌学
生物化学
基因
作者
Jiping Sun,Jing Wang,Wei Lu,Liyi Xie,Jing Lv,Huixian Li,Shifeng Yang
标识
DOI:10.1111/1440-1681.13371
摘要
Abstract Diabetic nephropathy (DN), a common cardiovascular disease, has been a global health threat. MicroRNAs (miRNAs) have been proposed to frequently participate in the occurrence and development of DN, however, the role of miR‐325‐3p in DN remains uncharacterized. Our research aimed to explore the function and mechanism of miR‐325‐3p in DN. Bioinformatics analysis (Targetscan, http://www.targetscan.org ) and a wide range of experiments including RT‐qPCR, CCK‐8 assay, western blot, luciferase reporter assay, RNA immunoprecipitation (RIP) assays, urine protein and blood glucose assays, histology analysis and morphometric analysis were used to explore the function and mechanism of miR‐325‐3p and C‐C motif chemokine ligand 19 (CCL19). CCL19 could facilitate the progression of DN by inhibiting cell viability and promoting inflammation and fibrosis in HK‐2 and HMC cells. In addition, CCL19 was confirmed to be targeted and negatively regulated by miR‐325‐3p. Rescue assays validated that the impacts of miR‐325‐3p mimics on the viability, inflammation and fibrosis of HK‐2 and HMC cells were recovered by CCL19 overexpression. To sum up, miR‐325‐3p inhibits renal inflammation and fibrosis by targeting CCL19 in a DN cell model and mice model, implying miR‐325‐3p as a possible therapeutic target for DN treatment.
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