LncRNA LOC103694972 promotes fibrosis of NRK-49F cells by regulating STAT3-dependent Smad/CTGF pathway via targeting miR-29c-3p  

作　　者：YAN LI HUZHI CAI XIAOLING PENG YOUHUI LIU QINGYANG CHEN XIANGDONG LIN XINYU CHEN 

机构地区：[1]Department of Vascular and Tumor Intervention,The First Hospital of Hunan University of Chinese Medicine,Changsha,410007,China [2]Department of Intensive Care Unit,The First Hospital of Hunan University of Chinese Medicine,Changsha,410007,China [3]Department of Nursing Research,The First Hospital of Hunan University of Chinese Medicine,Changsha,410007,China [4]Department of Intensivie Care Unit,The First Hospital of Hunan University of Chinese Medicine,Changsha,410007,China [5]Department of Endocrinology,The First Hospital of Hunan University of Chinese Medicine,Changsha,410007,China [6]Department of Preventive Treatment Center,The First Hospital of Hunan University of Chinese Medicine,Changsha,410007,China

出　　处：《BIOCELL》2024年第3期501-511,共11页生物细胞（英文）

基　　金：This work was supported by the Hunan Provincial Education Department General Project Research Fund(No.20C1412);the Hunan Graduate Scientific Research Innovation Project(No.CX2018B474);the National Famous Elderly Chinese Medicine Experts Xinyu Chen Inheritance Workshop Construction Project(No.[2022]75).

摘　　要：Background:Renalfibrosis is an important process in the development of chronic kidney disease.Understanding the pathogenesis andfinding effective treatments for renalfibrosis is crucial.This study aims to investigate whether a newly discovered long non-coding RNA(lncRNA)called LOC103694972 could be a potential target for treatingfibrosis of NRK-49F cells.Methods:LncRNA Chip was used to identify differentially expressed lncRNAs between TGF-β1-induced NRK-49F cells and normal cells.The dual-luciferase assay confirmed the binding between miR-29c-3p and signal transducer and activator of transcription(STAT3),as well as between miR-29c-3p and lncRNA LOC103694972.Si-LOC103694972 and miR-29c-3p mimic were then transfected into TGF-β1-induced NRK-49F cells.Results:The study found that LOC103694972 was highly expressed in TGF-β1-induced NRK-49F cells.These cells exhibited increased cell length and activity compared to the control group.The expression levels of Collagen I,α-Smooth muscle actin(α-SMA),and tissue inhibitor of metalloproteinase(TIMP-1)were increased,while matrix Metalloproteinase 2(MMP2)and matrix Metalloproteinase 9(MMP9)expression was decreased.However,transfection with si-LOC103694972 and miR-29c-3p mimics restored cell morphology and reduced cell viability.This led to a decrease in the levels of Collagen I,α-SMA,and TIMP-1,as well as an increase in MMP2 and MMP9 expression.Additionally,TGF-β1-induced NRK-49F cells transfected with miR-29c-3p mimics activated the STAT3-Smad3/CTGF pathway.Conclusion:Based on thesefindings,lncRNA LOC103694972 shows promise as a target for treating renalfibrosis.It negatively regulates miR-29c-3p and activates the STAT3-Smad3/CTGF pathway.

关 键 词：Renal fibrosis lncRNA LOC103694972 lncRNA Chip miR-29c-3p STAT3-Smad3/CTGF 

分 类 号：R692[医药卫生—泌尿科学]