Hui Liu, Yue Wang, Shuyuan Wang, Bo Yang, Di Sun, Shuangyang Han
{"title":"STUDY ON THE ROLE AND MECHANISM OF MICRORNA-650/WNT1 IN THE REPAIR OF ARTICULAR CARTILAGE INJURY.","authors":"Hui Liu, Yue Wang, Shuyuan Wang, Bo Yang, Di Sun, Shuangyang Han","doi":"10.1590/1413-785220243204e278218","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>Osteoarthritis (OA) is a degenerative disease associated with chondrocyte injury. This study investigated the dysregulation of microRNA-650 (miR-650) in cartilage tissues of patients with OA. Its function and mechanism were also investigated in OA cell models.</p><p><strong>Methods: </strong>miR-650 levels were examined in 15 OA cartilage tissues and ten healthy cartilage tissues. SW1353 cells were used for cell function experiments and IL-1β was applied to the cells to mimic OA conditions in vitro. Cell functions such as proliferation, apoptosis, and inflammation were detected. The downstream target gene of miR-650 was identified and confirmed by bioinformatic analysis and luciferase activity assay. Rescue experiments were performed to verify the mechanism.</p><p><strong>Results: </strong>Suppressed expression of miR-650 was tested in patients with OA and cell models. Overexpression of miR-650 increased cell proliferation but suppressed apoptosis and inflammation of SW1353. As the target gene of miR-650, WNT1 overexpression counteracted the role of miR-650 in the function of SW1353.</p><p><strong>Conclusion: </strong>miR-650 can protect against articular cartilage injury in OA by targeting WNT1. <b><i>Level of Evidence I, Experimental Study.</i></b></p>","PeriodicalId":55563,"journal":{"name":"Acta Ortopedica Brasileira","volume":"32 4","pages":"e278218"},"PeriodicalIF":0.5000,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11460656/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta Ortopedica Brasileira","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1590/1413-785220243204e278218","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q4","JCRName":"ORTHOPEDICS","Score":null,"Total":0}
引用次数: 0
Abstract
Objectives: Osteoarthritis (OA) is a degenerative disease associated with chondrocyte injury. This study investigated the dysregulation of microRNA-650 (miR-650) in cartilage tissues of patients with OA. Its function and mechanism were also investigated in OA cell models.
Methods: miR-650 levels were examined in 15 OA cartilage tissues and ten healthy cartilage tissues. SW1353 cells were used for cell function experiments and IL-1β was applied to the cells to mimic OA conditions in vitro. Cell functions such as proliferation, apoptosis, and inflammation were detected. The downstream target gene of miR-650 was identified and confirmed by bioinformatic analysis and luciferase activity assay. Rescue experiments were performed to verify the mechanism.
Results: Suppressed expression of miR-650 was tested in patients with OA and cell models. Overexpression of miR-650 increased cell proliferation but suppressed apoptosis and inflammation of SW1353. As the target gene of miR-650, WNT1 overexpression counteracted the role of miR-650 in the function of SW1353.
Conclusion: miR-650 can protect against articular cartilage injury in OA by targeting WNT1. Level of Evidence I, Experimental Study.
期刊介绍:
A Revista Acta Ortopédica Brasileira, órgão oficial do Departamento de Ortopedia e Traumatologia da Faculdade de Medicina da Universidade de São Paulo (DOT/FMUSP), é publicada bimestralmente em seis edições ao ano (jan/fev, mar/abr, maio/jun, jul/ago, set/out e nov/dez) com versão em inglês disponível nos principais indexadores nacionais e internacionais e instituições de ensino do Brasil. Sendo hoje reconhecidamente uma importante contribuição para os especialistas da área com sua seriedade e árduo trabalho para as indexações já conquistadas.