Epigenetic Mechanisms and Non-coding RNAs in Osteoarthritis

被引:59
作者
Barter, Matt J. [1 ]
Young, David A. [1 ]
机构
[1] Newcastle Univ, Sch Med, Musculoskeletal Res Grp, Inst Cellular Med, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England
关键词
Osteoarthritis; Cartilage; Chondrocyte; Epigenetic; DNA methylation; CpG; microRNA; Non-coding RNA; Long non-coding RNA; miR-140; Chromatin; Histone; SirT1; HDAC; HDAC inhibitor; SOX9; HISTONE DEACETYLASE INHIBITORS; MATRIX-METALLOPROTEINASE; 13; HUMAN ARTICULAR CHONDROCYTES; OXIDE SYNTHASE EXPRESSION; II COLLAGEN EXPRESSION; DNA METHYLATION; RHEUMATOID-ARTHRITIS; MICRORNA EXPRESSION; NITRIC-OXIDE; CPG SITES;
D O I
10.1007/s11926-013-0353-z
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Osteoarthritis (OA) is a disease typified by the loss of cartilage, the normal integrity of which is maintained by the resident cell, the chondrocyte. Alterations in chondrocyte gene expression with age, injury, loading or predisposing genetics, underpin OA cartilage loss. Cell- and tissue-specific gene expression is determined by epigenetic mechanisms, including DNA methylation, chromatin modifications and non-coding RNAs, including microRNAs and long-non-coding RNAs. A number of epigenetic changes have been identified between OA and normal cartilage, and the enzymes which impart the epigenetic code are increasingly seen as important players in a number of pathologies, including OA. Here, we will describe current and potential new epigenetic studies that are likely to reveal novel aspects of chondrocyte and cartilage biology and potentially help sub-characterise OA phenotypes. Importantly, many of these epigenetic modifiers or non-coding RNAs are proposed drug targets and could represent a therapeutic opportunity for this currently untreatable disease.
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页数:9
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