{"title":"miR-29c Carried by Lipid Nanoparticles Mediates TGF-β Signaling Pathway in Renal Fibrosis","authors":"Yuting Gong, Yumei Liang, Yinyin Chen, Ying Chen, Qinghua Zeng, Shuyi Qian","doi":"10.1166/jbn.2023.3711","DOIUrl":null,"url":null,"abstract":"miR-29c is related to renal fibrosis. Lipid nanoparticles can inhibit cell growth. This study mainly explores whether miR-29c carried by lipid nanoparticles may regulate the expression of TGF-β signaling and then involves in renal fibrosis. Kidney fibrosis cells HK-2 were intervened with 20 μmol/L miR-29c carried by lipid nanoparticles followed by analysis of the proliferation number and cell cycle changes of HK-2 cells, expression of TGF-β pathway protein, and relationship between TGF-β and miR-29c. Mice were infused with Ang II (1000 ng/kg/min) for 4 weeks to establish a mouse model of renal fibrosis. After treatment with miR-29c carried by lipid nanoparticles and PBS, the changes of renal fibrosis and the expression of TGF-β were measured. The higher the concentration of miR-29c carried by lipid nanoparticles, the more significant the decrease in cell proliferation, and cells in S phase began to decline significantly (P <0.05). Cell number in lipid nanoparticle+PBS group was the lowest and cells in PBS group and lipid nanoparticle+TGF-β inhibitor group were higher. TGF-β is a target gene of miR-29c. When the concentration of miR-29c in lipid nanoemulsion was 20 μmol/L, the expression of TGF-β protein decreased. miR-29c-carried lipid nanoparticles significantly attenuated Ang II-induced kidney injury. TGF-β was highly expressed in renal fibrosis compared with control mice and the expression of TGF-β was decreased after lipid nanoparticle treatment. miR-29c carried by lipid nanoparticles can inhibit the proliferation of renal fibrosis cells, regulate the TGF-β pathway, and ultimately control abnormal cell proliferation.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":"252 3 1","pages":""},"PeriodicalIF":2.9000,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of biomedical nanotechnology","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1166/jbn.2023.3711","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
miR-29c is related to renal fibrosis. Lipid nanoparticles can inhibit cell growth. This study mainly explores whether miR-29c carried by lipid nanoparticles may regulate the expression of TGF-β signaling and then involves in renal fibrosis. Kidney fibrosis cells HK-2 were intervened with 20 μmol/L miR-29c carried by lipid nanoparticles followed by analysis of the proliferation number and cell cycle changes of HK-2 cells, expression of TGF-β pathway protein, and relationship between TGF-β and miR-29c. Mice were infused with Ang II (1000 ng/kg/min) for 4 weeks to establish a mouse model of renal fibrosis. After treatment with miR-29c carried by lipid nanoparticles and PBS, the changes of renal fibrosis and the expression of TGF-β were measured. The higher the concentration of miR-29c carried by lipid nanoparticles, the more significant the decrease in cell proliferation, and cells in S phase began to decline significantly (P <0.05). Cell number in lipid nanoparticle+PBS group was the lowest and cells in PBS group and lipid nanoparticle+TGF-β inhibitor group were higher. TGF-β is a target gene of miR-29c. When the concentration of miR-29c in lipid nanoemulsion was 20 μmol/L, the expression of TGF-β protein decreased. miR-29c-carried lipid nanoparticles significantly attenuated Ang II-induced kidney injury. TGF-β was highly expressed in renal fibrosis compared with control mice and the expression of TGF-β was decreased after lipid nanoparticle treatment. miR-29c carried by lipid nanoparticles can inhibit the proliferation of renal fibrosis cells, regulate the TGF-β pathway, and ultimately control abnormal cell proliferation.