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| Regulation of commicroRNA-22 on chondrocyte senescence by inhibiting SIRT1 expression |
| YAN Shiju1, DONG Wenjing2, LI Zhirui1, ZHAO Yanpeng3, HAN Tao1, WEI Junqiang1, WANG Junliang1, LIN Feng1 |
1. Department of Orthopedics;
2. Department of Gerontology, Hainan Hospital of Chinese PLA General Hospital, Sanya 572013, China;
3. Department of Orthopedics, the Fourth Medical Center of Chinese PLA General Hospital, Beijing 100048, China |
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Abstract Objective To investigate the effects of microRNA-22 on chondrocyte senescence in osteoarthritis. Methods Primary chondrocytes were collected from OA cartilage and divided into miR-22 mimics group, miR-22 inhibitor group and Negative Control (NC) group, which were transfected with miR-22 mimics, miR-22 inhibitor and negative control respectively. MTT assay was used to detect the effects of microRNA-22 on cell proliferation of chondrocyte; senescence-associated β-galactosidase (SA-β-Gal) staining was performed to evaluate the effects of microRNA-22 on senescence of chondrocyte. Western blot was used to detect the expression level of SIRT1 and P16. Results Compared with Negative Control (NC) group, the proliferation rate of chondrocytes was significantly inhibited in miR-22 mimics group and upregulated in miR-22 inhibitor group. The ratio of SA-β-Gal-positive chondrocytes group was elevated in miR-22 mimics and downregulated in miR-22 inhibitor group. After chondrocytes were transfected with miR-22 mimics, the expression level of P16 was promoted while SIRT1 was inhibited. On the contrary, the expression level of P16 was decreased while SIRT1 was elevated after chondrocytes were transfected with miR-22 inhibitor. Conclusions For OA, microRNA-22 could inhibit chondrocyte proliferation, as well as promote chondrocyte senescence by regulating SIRT1 and P16, so microRNA-22 could be a novel target of OA treatment.
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Received: 06 July 2022
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2023, Vol. 34 
