Abstract
Osteoarthritis (OA), a chronic disease characterized by articular cartilage degeneration, is a leading cause of disability and pain worldwide. Accumulating evidence indicates that circular RNAs (circRNAs) play a critical role in various diseases, but the function of circRNAs in OA remains largely unknown. In this study, we found that circ_0001598 was significantly upregulated in chondrocytes treated with IL-1β and in cartilage tissue from mice with severed anterior cruciate ligament surgery (ACLT) induced OA models. Interference with circ_0001598 in vitro restored IL-1β-induced chondrocyte proliferation and apoptosis. Silencing circ_0001598 significantly alleviated ACLT-induced OA in mice. Mechanistically, knockdown of circ_0001598 affected chondrocyte proliferation, apoptosis, and matrix degradation by regulating miR-127-3p. Taken together, our results demonstrate the fundamental role of circ_0001598 and provide new ideas for the prevention and treatment of osteoarthritis.
Highlights
Osteoarthritis (OA) is one of the degenerative joint diseases with high teratogenic and disability rates in the world, which is mainly characterized by chondrocyte apoptosis and joint matrix degradation [1]. e incidence of OA mainly occurs in middle-aged and elderly people, and the clinical incidence increases gradually with the increase of age [2, 3]
Most people think that the occurrence and development of osteoarthritis are related to age, body weight, mechanical injury, and biological factors, and they may be related to biomechanical disorders caused by pathological changes of articular cartilage in vivo [6]. e occurrence and development of OA involve the whole cartilage tissue, of which the pathological changes are most closely related to cartilage tissue, and damage to cartilage tissue is closely related to chondrocyte apoptosis [7,8,9,10,11]
To investigate the in vivo role of circ_0001598 in the pathogenesis of OA, we injected circ_0001598 and control siRNA weekly for 4 weeks using articular cavity lentivirus in anterior cruciate ligament surgery (ACLT)-operated mice. qRT-PCR analysis was performed to verify the knockdown efficiency of circ_0001598 after lentivirus injection (Figure 3(a)). qRT-PCR and western blot showed that matrix metalloproteinase 13 (MMP-13) expression was increased, and COL2A1 expression was decreased in knee cartilage of mice with osteoarthritis, which was significantly alleviated by silencing circ_0001598 (Figures 3(b)–3(f))
Summary
Osteoarthritis (OA) is one of the degenerative joint diseases with high teratogenic and disability rates in the world, which is mainly characterized by chondrocyte apoptosis and joint matrix degradation [1]. e incidence of OA mainly occurs in middle-aged and elderly people, and the clinical incidence increases gradually with the increase of age [2, 3]. Most people think that the occurrence and development of osteoarthritis are related to age, body weight, mechanical injury, and biological factors, and they may be related to biomechanical disorders caused by pathological changes of articular cartilage in vivo [6]. Erefore, degradation of the extracellular matrix will lead to the change of mechanical properties of cartilage on the one hand and the loss of the survival environment of chondrocytes on the other hand, leading to apoptosis of chondrocytes [14]. Li et al stated that circ_0136474 increased in OA cartilage tissue and could inhibit chondrocyte proliferation and promote apoptosis [20]. Subsequent functional experiments showed that circ_0001598 significantly attenuated OA by binding miR-127-3p involved in chondrocyte proliferation, apoptosis, and matrix degradation. We revealed the fundamental role of circ_0001598 to provide a potential drug target for OA treatment
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