Long non-coding XIST raises methylation of TIMP-3 promoter to regulate collagen degradation in osteoarthritic chondrocytes after tibial plateau fracture

doi:10.1186/s13075-019-2033-5

科研成果详情

题名	Long non-coding XIST raises methylation of TIMP-3 promoter to regulate collagen degradation in osteoarthritic chondrocytes after tibial plateau fracture
作者	Chen, Hongwei 1; Yang, Shengdi 2; Shao, Ruyi 3
发表日期	2019-12-09
发表期刊	ARTHRITIS RESEARCH & THERAPY 影响因子和分区
语种	英语
原始文献类型	Article
关键词	Long noncoding RNA XIST TIMP-3 Methylation Osteoarthritis Chondrocytes Collagen degradation Tibial plateau fracture
其他关键词	AGGRECAN DEGRADATION ; EXPRESSION ; CARTILAGE ; ADAMTS-5 ; SPONGE ; REPAIR ; ASSAY
摘要	Background: Hypermethylation of gene promoters has been regarded as an epigenetic regulator for gene inactivation in the development of several diseases. In the current study, we aimed to explore how long noncoding RNA X-inactive specific transcript (lncRNA XIST) function in collagen degradation in chondrocytes of osteoarthritis (OA) after tibial plateau fracture by regulating tissue inhibitor of metalloproteinase-3 (TIMP-3) promoter methylation. Methods: In silico analysis was used to screen differentially expressed lncRNAs in cartilage tissues of OA. Chondrocytes were then successfully isolated from normal and OA cartilage tissues and identified, with the expressions of lncRNA XIST and TIMP-3 examined. The methylation levels of TIMP-3 promoter were determined by MS-PCR. The binding of lncRNA XIST to DNA methyltransferase and the binding of TIMP-3 promoter to DNA methyltransferase were determined by a series of experiments, including RIP, RNA pull-down, and ChIP assays. Results: The differentially expressed lncRNA XIST was determined in OA. In addition, cartilage tissues of OA showed upregulation of lncRNA XIST and downregulation of TIMP-3. LncRNA XIST was primarily localized in the nucleus and was capable of binding to the promoter of TIMP-3. The silencing of lncRNA XIST decreased the methylation levels of TIMP-3 promoter and increased the expressions of TIMP-3, which consequently inhibited collagen degradation in OA chondrocytes. Furthermore, TIMP-3 over-expression reversed the effect of lncRNA XIST on collagen degradation in OA chondrocytes. Conclusion: Collectively, lncRNA XIST raises collagen degradation in OA chondrocytes after tibial plateau fracture by accelerating the methylation of TIMP-3 promoter by recruiting DNA methyltransferase.
出版者	BMC
出版地	LONDON
ISSN	1478-6354
EISSN	1478-6362
卷号	21 期号:1 页码:271
DOI	10.1186/s13075-019-2033-5
页数	13
WOS类目	Rheumatology
WOS研究方向	Rheumatology
WOS记录号	WOS:000509120600001
收录类别	SCIE ; PUBMED ; SCOPUS
URL	查看原文
PubMed ID	31815654
PMC记录号	PMC6902347
SCOPUSEID	2-s2.0-85076305077
通讯作者地址	[Shao, Ruyi]Department of Orthopedics,Zhuji People's Hospital,No. 9, Jianmin Road,Zhuji, Zhejiang Province,311800,China
Scopus学科分类	Rheumatology;Immunology and Allergy;Immunology
TOP期刊	TOP期刊
引用统计	被引频次：15[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/4388
专题	其他_附属义乌医院（义乌市中心医院）第一临床医学院（信息与工程学院）、附属第一医院_外科学_整形外科
通讯作者	Shao, Ruyi
作者单位	1.Department of Orthopedic Surgery,Yiwu Central Hospital,Affiliated Yiwu Hospital of Wenzhou Medical University,Yiwu,322000,China; 2.Department of Hand-Foot Microsurgery,Lanshi Hospital,Lanzhou,730050,China; 3.Department of Orthopedics,Zhuji People's Hospital,No. 9, Jianmin Road,Zhuji, Zhejiang Province,311800,China
第一作者单位	附属义乌医院（义乌市中心医院）
第一作者的第一单位	附属义乌医院（义乌市中心医院）
推荐引用方式 GB/T 7714	Chen, Hongwei,Yang, Shengdi,Shao, Ruyi. Long non-coding XIST raises methylation of TIMP-3 promoter to regulate collagen degradation in osteoarthritic chondrocytes after tibial plateau fracture[J]. ARTHRITIS RESEARCH & THERAPY,2019,21(1):271.
APA	Chen, Hongwei, Yang, Shengdi, & Shao, Ruyi. (2019). Long non-coding XIST raises methylation of TIMP-3 promoter to regulate collagen degradation in osteoarthritic chondrocytes after tibial plateau fracture. ARTHRITIS RESEARCH & THERAPY, 21(1), 271.
MLA	Chen, Hongwei,et al."Long non-coding XIST raises methylation of TIMP-3 promoter to regulate collagen degradation in osteoarthritic chondrocytes after tibial plateau fracture".ARTHRITIS RESEARCH & THERAPY 21.1(2019):271.