Molecular mechanisms of the cartilage-specific microRNA-140 in osteoarthritis
- 993 Downloads
Osteoarthritis (OA) is the most widespread chronic degenerative joint disorder, characterized by progressive destruction of articular cartilage, subchondral bone alterations, formation of osteophytes and synovitis. MicroRNAs (miRNAs) are a class of endogenous and non-coding single-strand RNAs with a length of about 22 nucleotides, and many of them are evolutionarily conserved. miRNAs have been implicated in the process of development and pathogenesis of diseases, and tissue-specific miRNA functional studies in mice have revealed both pathogenic and protective functions. miRNA-140 (miR-140) was shown to be specifically expressed in cartilage tissues in developing zebrafish and mouse embryos during the development of both long and flat bones. Recently, miR-140 has been reported in many studies to play significant roles in OA pathogenesis. Although the previous results were not always consistent, the molecular mechanisms of the regulation and dual function of miR-140 in cartilage homeostasis and development have been established in previous studies. Further elucidation of the molecular basis of miR-140 will uncover synergistic inhibitory effects of miR-140 and other factors on OA pathogenesis, and provide a novel means of treating OA disease.
KeywordsMicroRNA-140 Cartilage Osteoarthritis
This study was supported by funding from the National Natural Science Foundation of China (No. 81272023, No. 81271948, No. 81201426, No. 81201373); the Key Project of International Scientific Cooperation of Shaanxi Province (No. 2013KW25-02) and the Fundamental Research Funds for the Central Universities (No. 2012JDGZ07, No. XJJ2012124).
- 36.Clemmons DR, Busby WH Jr, Garmong A, Schultz DR, Howell DS, Altman RD, et al. Inhibition of insulin-like growth factor binding protein 5 proteolysis in articular cartilage and joint fluid results in enhanced concentrations of insulin-like growth factor 1 and is associated with improved osteoarthritis. Arthritis Rheum. 2002;46:694–703.PubMedCrossRefGoogle Scholar