Inflammation and epigenetic regulation in osteoarthritis

被引:279
作者
Shen, Jie [1 ]
Abu-Amer, Yousef [1 ,2 ]
O'Keefe, Regis J. [1 ]
McAlinden, Audrey [1 ,2 ]
机构
[1] Washington Univ, Sch Med, Dept Orthopaed Surg, 660 Euclid Ave,CB 8233, St Louis, MO 63110 USA
[2] Washington Univ, Sch Med, Dept Cell Biol & Physiol, St Louis, MO 63110 USA
基金
美国国家卫生研究院;
关键词
DNA methylation; epigenetics; histone modification; inflammation; non-coding RNA; osteoarthritis; NF-KAPPA-B; LONG NONCODING RNAS; HUMAN ARTICULAR CHONDROCYTES; WIDE DNA METHYLATION; GENE-EXPRESSION; CPG SITES; RHEUMATOID-ARTHRITIS; MICRORNA EXPRESSION; ANABOLIC CYTOKINES; MMP EXPRESSION;
D O I
10.1080/03008207.2016.1208655
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Osteoarthritis (OA) was once defined as a non-inflammatory arthropathy, but it is now well-recognized that there is a major inflammatory component to this disease. In addition to synovial cells, articular chondrocytes and other cells of diarthrodial joints are also known to express inflammatory mediators. It has been proposed that targeting inflammation pathways could be a promising strategy to treat OA. There have been many reports of cross-talk between inflammation and epigenetic factors in cartilage. Specifically, inflammatory mediators have been shown to regulate levels of enzymes that catalyze changes in DNA methylation and histone structure, as well as alter levels of non-coding RNAs. In addition, expression levels of a number of these epigenetic factors have been shown to be altered in OA, thereby suggesting potential interplay between inflammation and epigenetics in this disease. This review provides information on inflammatory pathways in arthritis and summarizes published research on how epigenetic regulators are affected by inflammation in chondrocytes. Furthermore, we discuss data showing how altered expression of some of these epigenetic factors can induce either catabolic or anti-catabolic effects in response to inflammatory signals. A better understanding of how inflammation affects epigenetic factors in OA may provide us with novel therapeutic strategies to treat this condition.
引用
收藏
页码:49 / 63
页数:15
相关论文
共 167 条
[1]
Silencing microRNA-34a inhibits chondrocyte apoptosis in a rat osteoarthritis model in vitro [J].
Abouheif, Mohamed M. ;
Nakasa, Tomoyuki ;
Shibuya, Hayatoshi ;
Niimoto, Takuya ;
Kongcharoensombat, Wirat ;
Ochi, Mitsuo .
RHEUMATOLOGY, 2010, 49 (11) :2054-2060
[2]
NF-κB signaling and bone resorption [J].
Abu-Amer, Y. .
OSTEOPOROSIS INTERNATIONAL, 2013, 24 (09) :2377-2386
[3]
The tumor-suppressive and potential therapeutic functions of miR-34a in epithelial carcinomas [J].
Adams, Brian D. ;
Parsons, Christine ;
Slack, Frank J. .
EXPERT OPINION ON THERAPEUTIC TARGETS, 2016, 20 (06) :737-753
[4]
Circulating microRNAs as Potential Biomarkers in Non-Alcoholic Fatty Liver Disease and Hepatocellular Carcinoma [J].
Afonso, Marta B. ;
Rodrigues, Pedro M. ;
Simao, Andre L. ;
Castro, Rui E. .
JOURNAL OF CLINICAL MEDICINE, 2016, 5 (03)
[5]
MicroRNA-199a* regulates the expression of cyclooxygenase-2 in human chondrocytes [J].
Akhtar, Nahid ;
Haqqi, Tariq M. .
ANNALS OF THE RHEUMATIC DISEASES, 2012, 71 (06) :1073-1080
[6]
microRNAs: Tiny regulators with great potential [J].
Ambros, V .
CELL, 2001, 107 (07) :823-826
[7]
NF-κB, Inflammation, and Metabolic Disease [J].
Baker, Rebecca G. ;
Hayden, Matthew S. ;
Ghosh, Sankar .
CELL METABOLISM, 2011, 13 (01) :11-22
[8]
MicroRNAs: Target Recognition and Regulatory Functions [J].
Bartel, David P. .
CELL, 2009, 136 (02) :215-233
[9]
MicroRNAs: Genomics, biogenesis, mechanism, and function (Reprinted from Cell, vol 116, pg 281-297, 2004) [J].
Bartel, David P. .
CELL, 2007, 131 (04) :11-29
[10]
Epigenetic mechanisms in cartilage and osteoarthritis: DNA methylation, histone modifications and microRNAs [J].
Barter, M. J. ;
Bui, C. ;
Young, D. A. .
OSTEOARTHRITIS AND CARTILAGE, 2012, 20 (05) :339-349