{"title":"LncRNA-HHCP5调控ceRNA和m6A通路的KLF5抑制骨关节炎的进展","authors":"Peng Jiang, Yuxuan Song, Pengfei Li, Yanhui Yang, Jiyang Zhang","doi":"10.1111/1756-185X.70035","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Osteoarthritis (OA) is one of the most common bone disorders and has a serious impact on the quality of life of patients. LncRNA-HCP5 (HCP5) is downregulated in OA tissues. However, the latent function and regulatory mechanisms of HCP5 in OA are unclear.</p><p><strong>Methods: </strong>In the current study, IL-1β-induced C28/I2 cells were used to establish an in vitro model of OA. The expression of HCP5 in OA cartilage tissue and in the in vitro model of OA was detected by RT-qPCR. Cell viability and apoptosis were assessed by CCK-8 and Annexin V-PI double staining. Western blotting was employed to detect the protein expression of MMP-13 and aggrecan.</p><p><strong>Results: </strong>The results showed that the findings suggested that HCP5 was downregulated in OA cartilage tissue and IL-1β-induced C28/I2 cells. HCP5 overexpression greatly enhanced IL-1β-induced proliferation of C28/I2 cells, as well as prevented cell apoptosis and degradation of extracellular matrix (ECM). Besides, we have shown that HCP5 is a ceRNA that regulates KLF5 by sponging miR-375. Furthermore, KLF5 is also regulated by m6A regulation induced by HCP5. Finally, overexpression of miR-375, the m6A modification inhibitor, as well as KLF5 inhibition reversed the impact of HCP5 on IL-1β-induced C28/I2 cells.</p><p><strong>Conclusion: </strong>In summary, the present study demonstrated that the HCP5/KLF5 axis inhibited the progression of osteoarthritis.</p>","PeriodicalId":14330,"journal":{"name":"International Journal of Rheumatic Diseases","volume":"28 1","pages":"e70035"},"PeriodicalIF":2.4000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"LncRNA-HHCP5 Regulates KLF5 in ceRNA and m6A Pathways to Inhibit the Progression of Osteoarthritis.\",\"authors\":\"Peng Jiang, Yuxuan Song, Pengfei Li, Yanhui Yang, Jiyang Zhang\",\"doi\":\"10.1111/1756-185X.70035\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Osteoarthritis (OA) is one of the most common bone disorders and has a serious impact on the quality of life of patients. LncRNA-HCP5 (HCP5) is downregulated in OA tissues. However, the latent function and regulatory mechanisms of HCP5 in OA are unclear.</p><p><strong>Methods: </strong>In the current study, IL-1β-induced C28/I2 cells were used to establish an in vitro model of OA. The expression of HCP5 in OA cartilage tissue and in the in vitro model of OA was detected by RT-qPCR. Cell viability and apoptosis were assessed by CCK-8 and Annexin V-PI double staining. Western blotting was employed to detect the protein expression of MMP-13 and aggrecan.</p><p><strong>Results: </strong>The results showed that the findings suggested that HCP5 was downregulated in OA cartilage tissue and IL-1β-induced C28/I2 cells. HCP5 overexpression greatly enhanced IL-1β-induced proliferation of C28/I2 cells, as well as prevented cell apoptosis and degradation of extracellular matrix (ECM). Besides, we have shown that HCP5 is a ceRNA that regulates KLF5 by sponging miR-375. Furthermore, KLF5 is also regulated by m6A regulation induced by HCP5. Finally, overexpression of miR-375, the m6A modification inhibitor, as well as KLF5 inhibition reversed the impact of HCP5 on IL-1β-induced C28/I2 cells.</p><p><strong>Conclusion: </strong>In summary, the present study demonstrated that the HCP5/KLF5 axis inhibited the progression of osteoarthritis.</p>\",\"PeriodicalId\":14330,\"journal\":{\"name\":\"International Journal of Rheumatic Diseases\",\"volume\":\"28 1\",\"pages\":\"e70035\"},\"PeriodicalIF\":2.4000,\"publicationDate\":\"2025-01-01\",\"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://doi.org/10.1111/1756-185X.70035\",\"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://doi.org/10.1111/1756-185X.70035","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"RHEUMATOLOGY","Score":null,"Total":0}
LncRNA-HHCP5 Regulates KLF5 in ceRNA and m6A Pathways to Inhibit the Progression of Osteoarthritis.
Background: Osteoarthritis (OA) is one of the most common bone disorders and has a serious impact on the quality of life of patients. LncRNA-HCP5 (HCP5) is downregulated in OA tissues. However, the latent function and regulatory mechanisms of HCP5 in OA are unclear.
Methods: In the current study, IL-1β-induced C28/I2 cells were used to establish an in vitro model of OA. The expression of HCP5 in OA cartilage tissue and in the in vitro model of OA was detected by RT-qPCR. Cell viability and apoptosis were assessed by CCK-8 and Annexin V-PI double staining. Western blotting was employed to detect the protein expression of MMP-13 and aggrecan.
Results: The results showed that the findings suggested that HCP5 was downregulated in OA cartilage tissue and IL-1β-induced C28/I2 cells. HCP5 overexpression greatly enhanced IL-1β-induced proliferation of C28/I2 cells, as well as prevented cell apoptosis and degradation of extracellular matrix (ECM). Besides, we have shown that HCP5 is a ceRNA that regulates KLF5 by sponging miR-375. Furthermore, KLF5 is also regulated by m6A regulation induced by HCP5. Finally, overexpression of miR-375, the m6A modification inhibitor, as well as KLF5 inhibition reversed the impact of HCP5 on IL-1β-induced C28/I2 cells.
Conclusion: In summary, the present study demonstrated that the HCP5/KLF5 axis inhibited the progression of osteoarthritis.
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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