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lncrna loc103694972 promotes fibrosis of NRK-49F cells by regulating STAT3-dependent Smad/CTGF pathway via targeting miR-29c-3p

引用

BIOCELL 2024年第3期48卷 501-511页

作者： YAN LI HUZHI CAI XIAOLING PENG YOUHUI LIU QINGYANG CHEN XIANGDONG LIN XINYU CHEN Department of Vascular and Tumor Intervention The First Hospital of Hunan University of Chinese MedicineChangsha410007China Department of Intensive Care Unit The First Hospital of Hunan University of Chinese MedicineChangsha410007China Department of Nursing Research The First Hospital of Hunan University of Chinese MedicineChangsha410007China Department of Intensivie Care Unit The First Hospital of Hunan University of Chinese MedicineChangsha410007China Department of Endocrinology The First Hospital of Hunan University of Chinese MedicineChangsha410007China Department of Preventive Treatment Center The First Hospital of Hunan University of Chinese MedicineChangsha410007China

Background:Renalﬁbrosis is an important process in the development of chronic kidney *** the pathogenesis andﬁnding effective treatments for renalﬁbrosis is *** 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 ***:lncrna Chip was used to identify differentially expressed lncrnas between TGF-β1-induced NRK-49F cells and normal *** 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 and miR-29c-3p mimic were then transfected into TGF-β1-induced NRK-49F ***:The study found that loc103694972 was highly expressed in TGF-β1-induced NRK-49F *** cells exhibited increased cell length and activity compared to the control *** 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 ***,transfection with si-loc103694972 and miR-29c-3p mimics restored cell morphology and reduced cell *** led to a decrease in the levels of Collagen I,α-SMA,and TIMP-1,as well as an increase in MMP2 and MMP9 ***,TGF-β1-induced NRK-49F cells transfected with miR-29c-3p mimics activated the STAT3-Smad3/CTGF ***:Based on theseﬁndings,lncrna loc103694972 shows promise as a target for treating renalﬁ*** 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

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