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学科主题: 临床医学
题名:
Silencing of microRNA-101 prevents IL-1 beta-induced extracellular matrix degradation in chondrocytes
作者: Dai, Linghui1; Zhang, Xin1; Hu, Xiaoqing1; Zhou, Chunyan2; Ao, Yingfang1
刊名: ARTHRITIS RESEARCH & THERAPY
发表日期: 2012
DOI: 10.1186/ar4114
卷: 14, 期:6
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Rheumatology
研究领域[WOS]: Rheumatology
关键词[WOS]: HUMAN ARTICULAR CHONDROCYTES ; GENE-EXPRESSION ; IMMUNE-SYSTEM ; COLLAGEN GENE ; MESSENGER-RNA ; II COLLAGEN ; SOX9 ; CARTILAGE ; OSTEOARTHRITIS ; ARTHRITIS
英文摘要:

Introduction: Extracellular matrix (ECM) degradation leads to malfunction of the cartilage in osteoarthritis (OA). Inflammatory cytokine interleukin-1 beta (IL-1 beta) functions in ECM degradation and prevents ECM synthesis by down-regulating the key transcription factor, Sox9, and consequently inhibiting ECM gene expression. Evidence reveals that microRNAs (miRNA) have been associated with OA, but little is known of their function in chondrocyte ECM degradation. This study aimed to identify possible miRNAs that mediate IL-1 beta-induced down-regulation of Sox9 as well as its known down-stream genes, collagen type II and aggrecan.

Methods: The miRNAs were predicted based on three classical databases. The expression levels of the predicted miRNAs were assessed in IL-1 beta stimulated chondrocytes by real-time PCR. A luciferase reporter was used to test the binding of the miRNAs to the 3′ untranslated regions (3′UTR) of Sox9. The predicted miRNAs were transfected into chondrocytes to validate their relationship with Sox9. Functional analysis of the miRNAs on chondrocytes ECM degradation was performed at both the mRNA and protein levels after miRNA transfection and IL-1 beta treatment.

Results: Six miRNAs were predicted to target Sox9, and their expression in IL-1 beta-stimulated chondrocytes was revealed by real-time PCR. The luciferase reporter assay indicated that only miR-101 could bind to the 3′ UTR of Sox9. The expression of Sox9 was likewise negatively regulated by miR-101 in rat chondrocytes. Functional analysis showed that miR-101 could aggravate chondrocyte ECM degradation, whereas miR-101 inhibition could reverse IL-1 beta-induced ECM degradation.

Conclusion: miR-101 participates in IL-1 beta-induced chondrocyte ECM degradation. Down-regulating miR-101 expression can prevent the IL-1 beta-induced ECM degradation in chondrocytes. miR-101 probably functions by directly targeting Sox9 mRNA.

语种: 英语
所属项目编号: 90919022 ; bmu2009129-112 ; 20110001130001
项目资助者: National Natural Science Foundation of China ; Ministry of Health of the People&prime ; s Republic of China ; Specialized Research Fund for the Doctoral Program of Higher Education
WOS记录号: WOS:000315192300044
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/64104
Appears in Collections:北京大学第三临床医学院_运动医学研究所_期刊论文

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作者单位: 1.Peking Univ, Hosp 3, Inst Sports Med, Beijing 100191, Peoples R China
2.Peking Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, Beijing 100191, Peoples R China

Recommended Citation:
Dai, Linghui,Zhang, Xin,Hu, Xiaoqing,et al. Silencing of microRNA-101 prevents IL-1 beta-induced extracellular matrix degradation in chondrocytes[J]. ARTHRITIS RESEARCH & THERAPY,2012,14(6).
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