IL16 Regulates Osteoarthritis Progression as a Target Gene of Novel-miR-81.

IF 2.7 4区医学 Q1 ORTHOPEDICS CARTILAGE Pub Date : 2024-06-01 Epub Date: 2023-04-21 DOI:10.1177/19476035231168387

Ziwei Luo, Qianting Han, Jianghua Lu, Xiyan Ouyang, Yueying Fan, Yangping Liu, Xianxi Zhou, Jiechen Kong, Helu Liu, Aijun Liu, Dongfeng Chen

{"title":"IL16 Regulates Osteoarthritis Progression as a Target Gene of Novel-miR-81.","authors":"Ziwei Luo, Qianting Han, Jianghua Lu, Xiyan Ouyang, Yueying Fan, Yangping Liu, Xianxi Zhou, Jiechen Kong, Helu Liu, Aijun Liu, Dongfeng Chen","doi":"10.1177/19476035231168387","DOIUrl":null,"url":null,"abstract":"Objective: Functional polymorphisms of interleukin 16 (IL16) have been reported to be closely related to the risk of osteoarthritis (OA). However, how IL16 affects OA remains unclear. In this study, the role of IL16 in OA and the possible mechanisms were examined.Methods: We established a meniscal/ligament injury (MLI) post-traumatic OA model in Sprague Dawley rats and an IL1β-induced ADTC5 cells OA model. We detected the expression of IL16, novel-miR-81, MMP3, and MMP13 by quantitative real-time polymerase chain reaction. Western blot was performed to detect the expression of IL16, MMP3, and MMP13. The association between IL16 and novel-miR-81 was confirmed by luciferase reporter assay. Hematoxylin and eosin staining, Safranin O and Fast Green staining, and immunohistochemical staining were performed to clarify the effect of intra-articular injection of novel-miR-81 agomir in rats OA model.Results: IL16 was upregulated in OA model. Knockdown of IL16 and overexpression of novel-miR-81 downregulated the expression of MMP3 and MMP13. Importantly, IL16 was a key target of novel-miR-81. Intra-articular injection of novel-miR-81 agomir could attenuate OA progression in rats OA model.Conclusion: Novel-miR-81 targeted IL16 to relieve OA, suggesting that novel-miR-81and IL16 may be new therapeutic targets for OA.","PeriodicalId":9626,"journal":{"name":"CARTILAGE","volume":null,"pages":null},"PeriodicalIF":2.7000,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11368893/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"CARTILAGE","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/19476035231168387","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/4/21 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"ORTHOPEDICS","Score":null,"Total":0}

引用次数: 0

Abstract

Objective: Functional polymorphisms of interleukin 16 (IL16) have been reported to be closely related to the risk of osteoarthritis (OA). However, how IL16 affects OA remains unclear. In this study, the role of IL16 in OA and the possible mechanisms were examined.

Methods: We established a meniscal/ligament injury (MLI) post-traumatic OA model in Sprague Dawley rats and an IL1β-induced ADTC5 cells OA model. We detected the expression of IL16, novel-miR-81, MMP3, and MMP13 by quantitative real-time polymerase chain reaction. Western blot was performed to detect the expression of IL16, MMP3, and MMP13. The association between IL16 and novel-miR-81 was confirmed by luciferase reporter assay. Hematoxylin and eosin staining, Safranin O and Fast Green staining, and immunohistochemical staining were performed to clarify the effect of intra-articular injection of novel-miR-81 agomir in rats OA model.

Results: IL16 was upregulated in OA model. Knockdown of IL16 and overexpression of novel-miR-81 downregulated the expression of MMP3 and MMP13. Importantly, IL16 was a key target of novel-miR-81. Intra-articular injection of novel-miR-81 agomir could attenuate OA progression in rats OA model.

Conclusion: Novel-miR-81 targeted IL16 to relieve OA, suggesting that novel-miR-81and IL16 may be new therapeutic targets for OA.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

IL16 作为 Novel-miR-81 的靶基因调控骨关节炎的进展

目的：据报道，白细胞介素 16（IL16）的功能多态性与骨关节炎（OA）的发病风险密切相关。然而，IL16 如何影响 OA 仍不清楚。本研究探讨了 IL16 在 OA 中的作用及其可能的机制：方法：我们在 Sprague Dawley 大鼠中建立了半月板/韧带损伤（MLI）后创伤性 OA 模型和 IL1β 诱导的 ADTC5 细胞 OA 模型。我们通过实时定量聚合酶链反应检测了 IL16、novel-miR-81、MMP3 和 MMP13 的表达。通过 Western 印迹检测 IL16、MMP3 和 MMP13 的表达。荧光素酶报告实验证实了 IL16 与新型 miR-81 之间的关联。为了明确在大鼠 OA 模型中关节内注射新型-miR-81 激动剂的效果，还进行了苏木精和伊红染色、沙弗林 O 和快绿染色以及免疫组化染色：结果：IL16在OA模型中上调。结果：IL16 在 OA 模型中上调，敲除 IL16 和过表达 novel-miR-81 会降低 MMP3 和 MMP13 的表达。重要的是，IL16 是 novel-miR-81 的一个关键靶点。在大鼠 OA 模型中，关节内注射新型-miR-81 激动剂可减轻 OA 的进展：结论：novel-miR-81可靶向IL16缓解OA，这表明novel-miR-81和IL16可能是OA的新治疗靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

CARTILAGE ORTHOPEDICS-

CiteScore

6.90

自引率

7.10%

发文量

期刊介绍： CARTILAGE publishes articles related to the musculoskeletal system with particular attention to cartilage repair, development, function, degeneration, transplantation, and rehabilitation. The journal is a forum for the exchange of ideas for the many types of researchers and clinicians involved in cartilage biology and repair. A primary objective of CARTILAGE is to foster the cross-fertilization of the findings between clinical and basic sciences throughout the various disciplines involved in cartilage repair. The journal publishes full length original manuscripts on all types of cartilage including articular, nasal, auricular, tracheal/bronchial, and intervertebral disc fibrocartilage. Manuscripts on clinical and laboratory research are welcome. Review articles, editorials, and letters are also encouraged. The ICRS envisages CARTILAGE as a forum for the exchange of knowledge among clinicians, scientists, patients, and researchers. The International Cartilage Repair Society (ICRS) is dedicated to promotion, encouragement, and distribution of fundamental and applied research of cartilage in order to permit a better knowledge of function and dysfunction of articular cartilage and its repair.