{"title":"SLC2A3在类风湿关节炎中的功能特征：揭示其在铁下垂和炎症途径中的作用。","authors":"Zhiping Lin, Peng Li, Chaojun Wang, Hongchang Tan","doi":"10.1111/1756-185X.70009","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Background</h3>\n \n <p>Hence, we investigated that the function and effects of SLC2A3 in rheumatoid arthritis (RA) and the underlying mechanism.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>C57BL/6 mice were immunized with bovine type II collagen to induce mice model of RA.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>The expression of serum SLC2A3 was down-regulated, and was negative correlation with CRP, RF or anti-CCP in patients with RA. In mice model of RA, SLC2A3 mRNA and protein expression in joint tissue were reduced. Sh-SLC2A3 promoted RA and inflammation in mice model. SLC2A3 promoted cell growth and osteogenic differentiation of MC3T3-E1 cells in vitro model of RA. SLC2A3 reduced ferroptosis in vitro model or mice model of RA. SLC2A3 induced Tiam1 protein expression, and SLC2A3 protein linked with Tiam1 protein in model of RA. Tiam1 reduced the effects of sh-SLC2A3 on RA and inflammation in mice model. Tiam1 inhibitor the effects of SLC2A3 on osteogenic differentiation and ferroptosis in vitro model of RA.</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p>Collectively, SLC2A3 reduced inflammation levels and ferroptosis through the inactivation of mitochondrial damage by Tiam1 in model of RA, could serve as a potent therapeutic agent for alleviating RA.</p>\n </section>\n </div>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"27 12","pages":""},"PeriodicalIF":2.4000,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Functional Characterization of SLC2A3 in Rheumatoid Arthritis: Unraveling Its Role in Ferroptosis and Inflammatory Pathways\",\"authors\":\"Zhiping Lin, Peng Li, Chaojun Wang, Hongchang Tan\",\"doi\":\"10.1111/1756-185X.70009\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Background</h3>\\n \\n <p>Hence, we investigated that the function and effects of SLC2A3 in rheumatoid arthritis (RA) and the underlying mechanism.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Methods</h3>\\n \\n <p>C57BL/6 mice were immunized with bovine type II collagen to induce mice model of RA.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>The expression of serum SLC2A3 was down-regulated, and was negative correlation with CRP, RF or anti-CCP in patients with RA. In mice model of RA, SLC2A3 mRNA and protein expression in joint tissue were reduced. Sh-SLC2A3 promoted RA and inflammation in mice model. SLC2A3 promoted cell growth and osteogenic differentiation of MC3T3-E1 cells in vitro model of RA. SLC2A3 reduced ferroptosis in vitro model or mice model of RA. SLC2A3 induced Tiam1 protein expression, and SLC2A3 protein linked with Tiam1 protein in model of RA. Tiam1 reduced the effects of sh-SLC2A3 on RA and inflammation in mice model. Tiam1 inhibitor the effects of SLC2A3 on osteogenic differentiation and ferroptosis in vitro model of RA.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Conclusions</h3>\\n \\n <p>Collectively, SLC2A3 reduced inflammation levels and ferroptosis through the inactivation of mitochondrial damage by Tiam1 in model of RA, could serve as a potent therapeutic agent for alleviating RA.</p>\\n </section>\\n </div>\",\"PeriodicalId\":14330,\"journal\":{\"name\":\"International Journal of Rheumatic Diseases\",\"volume\":\"27 12\",\"pages\":\"\"},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2024-12-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Journal of Rheumatic Diseases\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/1756-185X.70009\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"RHEUMATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Rheumatic Diseases","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/1756-185X.70009","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"RHEUMATOLOGY","Score":null,"Total":0}
Functional Characterization of SLC2A3 in Rheumatoid Arthritis: Unraveling Its Role in Ferroptosis and Inflammatory Pathways
Background
Hence, we investigated that the function and effects of SLC2A3 in rheumatoid arthritis (RA) and the underlying mechanism.
Methods
C57BL/6 mice were immunized with bovine type II collagen to induce mice model of RA.
Results
The expression of serum SLC2A3 was down-regulated, and was negative correlation with CRP, RF or anti-CCP in patients with RA. In mice model of RA, SLC2A3 mRNA and protein expression in joint tissue were reduced. Sh-SLC2A3 promoted RA and inflammation in mice model. SLC2A3 promoted cell growth and osteogenic differentiation of MC3T3-E1 cells in vitro model of RA. SLC2A3 reduced ferroptosis in vitro model or mice model of RA. SLC2A3 induced Tiam1 protein expression, and SLC2A3 protein linked with Tiam1 protein in model of RA. Tiam1 reduced the effects of sh-SLC2A3 on RA and inflammation in mice model. Tiam1 inhibitor the effects of SLC2A3 on osteogenic differentiation and ferroptosis in vitro model of RA.
Conclusions
Collectively, SLC2A3 reduced inflammation levels and ferroptosis through the inactivation of mitochondrial damage by Tiam1 in model of RA, could serve as a potent therapeutic agent for alleviating RA.
期刊介绍：
The International Journal of Rheumatic Diseases (formerly APLAR Journal of Rheumatology) is the official journal of the Asia Pacific League of Associations for Rheumatology. The Journal accepts original articles on clinical or experimental research pertinent to the rheumatic diseases, work on connective tissue diseases and other immune and allergic disorders. The acceptance criteria for all papers are the quality and originality of the research and its significance to our readership. Except where otherwise stated, manuscripts are peer reviewed by two anonymous reviewers and the Editor.
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